![]() Calories are units of energy. Various definitions exist but fall into two broad categories. The small calorie or gram calorie (symbol: cal) is the approximate amount of energy needed to raise the temperature of one gram of water by one degree Celsius at a pressure. Calorie Deficit Calculator This Calorie Deficit Calculator will determine the estimated total number of calories you need to maintain your current weight based on your BMR. 4 Ways To Ruin Your Calorie Deficit Article by JC Deen . If this is at 10 a.m., you Weight Loss 101: How to Calculate a Calorie Deficit Weight Loss 101: How to Calculate a Calorie Deficit By Matt Fitzgerald For Active.com To lose weight, you have to eat fewer calories than your body burns each day. It seems simple enough. Home / Planning / Calorie Deficit to Meet Weight Loss Goals / Losing Weight Calculator This calculator will estimate your daily calorie requirements for losing. Understanding Calories vs. Quality of Diet Does it matter where your calories come from? Is it better to get most of your calories from protein, or eat fewer calories from carbs? Experts have argued on this topic for some time, but the answer is simple: a calorie is. ![]() Hussman Fitness - The Scale: Caloric Deficits and Fat Loss. Caloric Deficits and Fat Loss By John P. Hussman, Ph. D. All rights reserved and actively enforced. The secret to fat loss is simple. If you accumulate persistent caloric deficits day after day, you will lose fat. It's a law of physics. My main page, http: //www. A complete program includes resistance training, aerobic training, interval training (get winded and recover, get winded and recover), cross training (alternating two different exercises on different days, e. Proper supplementation, particularly post- workout whey protein or leucine, is helpful (see my main page). Calculate Calorie Deficit to Reach Goal Weight Calculators 2 Comments 103 Simply enter you current weight, your goal weight and the time in which you wish to achieve the weight loss and click calculate (use this BMR calculator to determine your baseline. What's Your Diet Deficit? Many fad diets leave out more than the carbs, fat, or extra calories. From the WebMD Archives. Any diet that keeps you at a very low number of calories can be a problem, even if you're eating healthy food. Rapid weight loss on any. Lots of water and sufficient rest are also a must. These are proven techniques that can transform your body and improve your fitness level. ![]() Unfortunately many so- called weight loss strategies are really muscle loss strategies. These include severe restriction of carbohydrates (the Atkins diet, for example) and excessive training without proper post- exercise nutrition. Eating too much in the way of simple, processed carbohydrates (white flour, sugar) also kicks up insulin, which prevents fat burning until the insulin clears the system (which can take a while if you've got insulin regulation problems). My hope is that the information on this site will help you succeed while avoiding the pitfalls. ![]() While the components of a proper fitness program may seem like an overwhelming list, they're actually very simple when you break them down into daily actions. Before you begin - Know how to measure progress If your goal is fat loss, the scale is an extremely poor tool for measuring progress, particularly when you are doing any kind of weight training. Also, there is so much variation in water retention and digestive contents that you really cannot get a useful reading until your fat loss is significant as a percentage of your body weight. The mirror is another poor measuring tool. Fat never spot- reduces. It comes off in proportion to the existing fat layer. This is why you can estimate your body fat percentage by measuring the skinfold at just one or two locations (The clunky but consistent Slim Guide caliper is about $2. I prefer it to electronic gadgets, which can be very temperamental. You can interpret your suprailiac readings using my caliper calculator: http: //www. Usually, the shoulders and upper body are the first to show visual improvement, since these are the areas where the fat layer is thinnest. But the progress will come if you don't give up. The way to measure fat loss is to use a combination of tools, and to focus on trends rather than single isolated readings. You should use waist circumference, the fit of your clothes, skinfold caliper readings, and changes in your trough- to- trough weight readings over a period of time. For instance, if you weigh yourself daily (preferably in the morning) your day to day readings will bounce up and down. I generally track the 7- day average of fat mass (body fat percentage times scale weight), which has fewer jumps and stalls. In short, don't approach your fitness program demanding daily proof from the scale or the mirror. Go ahead and take measurements, but understand that there is day- to- day noise in those measurements from water retention, digestive contents and other factors that can be as much as 4% of total body weight. You have to take day- to- day fluctuations with a grain of salt and focus on a combination of readings from clothes, scale, calipers, and other tools. I really believe that the key to success in nearly everything is DAILY ACTION. Find a combination of actions that you are confident will bring success if you follow them consistently. Then follow them consistently. ![]() Low-Calorie Diet A low-calorie diet is usually used to achieve weight loss of 1 lb (0.5 kg) to 2 lb (0.9 kg) per week. Most experts do not recommend losing more than 2 lb (0.9 kg) per week unless you are participating in a medically-supervised weight loss plan. A diet that results in calorie deficit does not necessarily mean a quality diet, but it does mean weight loss. Store Top 50 Products Top 10 Product Lists Sales & Specials Clearance Products Categories Brands Goals Ingredients. The rest of this page is intended to prove to you why creating a persistent daily caloric deficit should be one of those actions. Some people do very well following a portion rule (5- 6 small meals a day, with a palm sized portion of protein and a palm sized portion of carbohydrate). But if that isn't working for you, it's time to track your caloric deficit directly. Caloric Deficits A caloric deficit is simply the number of calories you take in, minus the number of calories you burn. On the intake side, a good way to count calories is to think in terms of ingredients. A slice of bread is about 7. A medium potato or a medium cup of oatmeal or steamed rice is about 1. Dense, dry carbohydrates roughly double the calories (bagels, cereal or pretzels). A roasted skinless chicken breast is about 1. Frying anything roughly triples the calories, as does putting it in mayo (tuna salad). Anything prepared with fat automatically adds 1. The things that blow your calories out of control are fat, highly refined carbohydrates, and lack of water content. For the first few weeks, write down everything you eat - even those two grapes - immediately on a 3x. If you follow roughly the same meal plan every week, it is definitely worth the effort to carefully and honestly estimate the calories of your usual meals using a measuring cup and an inexpensive food scale. If you do this even once, you'll find that it's much easier to track your daily intake accurately. On the output side, click here to estimate your . Your BMR is the number of calories you'll typically burn lying in bed all day. If you work out solidly with weights for about 4. BMR that day. If you don't work out, but have a normal level of activity, you'll probably burn about 1. BMR. When scientists talk about . Every day, take the number of calories you take in, and subtract the number of calories you burn. If you're trying to lose weight, you want this to be a negative number - a . Your main goal for fat loss is to accumulate a significant caloric deficit over the entire week. If you're aggressively targeting fat loss, try to keep your caloric intake close to or slightly below your BMR (but not more than about 1. In order to lose 1 pound of fat, you've got to burn 3. This is true whether you have major fat loss goals (which was my challenge a couple of years ago), or whether your goal is maintenance and . My fat loss goal was modest: lose about 8- 1. What you see below is a chart of exactly how the fat came off. Specifically, there are two lines. The blue line is my cumulative fat loss. To get a reasonable fat estimate, I multiplied my morning scale weight times my body fat percentage to get . The red line is my cumulative caloric deficit (just a running total of the daily deficits, day by day), divided by 3. I used 1. 5 x BMR on workout days, but since I manage an investment company and work in front of trading screens all day, I used 1. BMR for free days. The graph below shows why a persistent caloric deficit is the key to fat loss. When I first looked at this graph, even I was surprised. I knew that fat loss was related to my caloric deficit. But I had no idea how close that relationship was. Take a look early in the graph where the lines both go above zero. Take a look near the end of the graph where they go up again. That's where I took a . Even with this smoothing, there are still points where the progress goes sideways for a while even though the deficits are accumulating. Then boom, both figures come back together. Too many people quit their fitness programs because the scale figures are unexpectedly high for a few days. Don't do this to yourself. Focus on daily actions. Create a persistent caloric deficit. The results will come. I hope that this helps!
0 Comments
Healthier Choices at Freebirds World Burrito. Soft corn tacos are a healthier choice at Freebirds World Burrito. Freebirds World Burrito is new to our town, so I decided to check them out and see what healthier options they might have. And thanks to the magic of the internet — and online nutritional information — I was able to do just that. Burritos the size of torpedos. I defeated the Super Monster only. Freebirds World Burrito. Are you trying to lose weight?Have you found the best weight loss diet in the USA?Here I have found the best weight loss. More full days of eating coming soon! As well as my 100 pound weight loss transformation coming out this month. Im exited to show you guys how losing weight is simply effortless and shouldn't be a dreadful process. Jenalys Carl is on Facebook. Freebirds World Burrito, ThunderCloud Subs. Tiff's Treats, Jardesca California Aperitiva, North Obgyn weight-loss I.P. Freebirds World Burrito. Tyghaman, Helena Bonham Carter, Ferb Fletcher, Cookie Monster. ![]() One of the great things about this place is that you have total control about what goes into your food, as it. The employees are extremely friendly, and there. ![]() ![]() Take a look at Freebirds World Burrito Cilantro related products and other millions of foods. Main; Food; Soups, Sauses. Product Overview; Nutrition Facts; Alternatives; How to burn; USER. A s 1 b s 2 c s 3 d s 4 21 the inverse demand for SCHOOL UCSB; COURSE TITLE ECON 100B; TYPE. PAGES 9 Click to edit the document details; This preview shows. So unless you want to split the small one, and go easy on the ingredients, it. I ordered them with soft corn tortillas, chicken (white meat), queso fresco, cilantro, corn relish and tomatoes. And although that was OK for a lunch as far as calories go (4. The next time I will omit the queso fresco to bring it down to a very manageable 3. Not bad for fast- food, which is usually very high in sodium. Another option would be the Freedom Salad, with lettuce, chicken, tomatoes, jalapenos, and corn salsa — with tomatillo dressing on the side. That clocks in at a very skinny 1. ![]() And it looks very filling. Either way, I will return to Freebirds World Burrito, as I can have it my way — the healthier way! Freebirds World Burrito* Whenever possible, I calculate ALL my Points on my website with my. Offline Points Calculator in the Half Points Mode, which rounds UP to the nearest Half Point. This keeps my site consistent. All point values in black bold are the new Points. Plus values,while all point values in red bold are the old Point values . Return to Restaurant Lists.
![]() The Rujuta Diet Plan . She has written a book, does private consultations and owns her own fitness studio. Though the specifics of a . ![]() Typically, those following Rujuta's diet plan to eat eight or nine meals per day. Eating small quantities throughout the day will prevent you from feeling overly hungry and gorging yourself in one sitting. Examples of meals include an apple, a serving of egg whites, muesli and milk, a slice of cheese and bread or a handful of nuts. Exercise at least one out of every 3. Rujuta calls this her . Exercise doesn't have to be anything extreme; a nice jog will do the trick. Celebrity fitness expert Rujuta Diwekar took questions from you, our dear readers, on how to stay fit. Rujuta Diwekar is out with her new book -- Don't Lose Out Work Out-- that deals with various workout-related myths. The celebrity fitness trainer, best known for her work with Kareena Kapoor and. Rujuta Diwekar Diet Plan For Weight Loss Best Detox Products To Cleanse My Body 7 Day Detox Miracle Peter Bennett 2 Day Drug Detox Total Body Detox Thc Burn Detox Pills Rujuta Diw. You should exercise to your limit, but not try to exceed it. She cites the example of two friends jogging: One might run for 6. Either is fine as long as the times reflect their respective abilities. Take daily supplements to ensure you get enough vitamins, minerals and omega- 3 fatty acids. Drink a lot of water, up to five liters- -about 2. Be aware that a cup of water can be different from a. ![]() ![]() ![]() ![]() In order to maintain healthy our body must have a healthy and balanced diet. This means we must eat sufficient food and also eat a variety of foods. Note that extra doses of some kinds of vitamins can be dangerous. ![]() A diet can easily be adequate for normal bodily functioning, yet may not be a balanced diet. An ideal human diet contains fat, protein, carbohydrates, vitamins, minerals, water and fibre all in correct proportions. These proportions vary for each individual because everyone has different metabolic rates and levels of activity. Malnutrition results from an unbalanced diet, this can be due to an excess of some dietary components and lack of other components, not just a complete lack of food. Too much of one component can be as much harm to the body as too little. Deficiency diseases occur when there is a lack of a specific nutrient, although some diet related disorders are a result of eating an excess. An adequate diet provides sufficient energy for the performance of metabolic work, although the energy food is in an unspecified form. A balanced diet provides all dietary requirements in the correct proportions. Ideally this would be 1/7 fat, 1/7 protein and 5/7 carbohydrate. Energy is provided by carbohydrates, fats and proteins. Balanced diet keeps our body fit and resistant to diseases. RDA is the Recommended Dietary Allowance which should be followed by individual in order to maintain good.Proteins are a provider of energy in an emergency, but are primarily used as building blocks for growth and repair of many body tissues. These energy providing compounds are needed in large quantities in our diet so are described as macronutrients. We also need much smaller amounts of other nutrients, such as vitamins and minerals. Because much smaller quantities are needed for a balanced diet these are known as micronutrients. Despite the small quantities needed these are essential to provide a healthy diet as they have specific roles in metabolic reactions and as structural components. Within the cells of our body, the nutrients ingested are converted to other compounds which are then used for metabolism and other cellular reactions. Starch, a major carbohydrate is converted to glucose which can be then synthesised into fat for storage, proteins are synthesised from amino acids, and phospholipids are made from glycerol and fatty acids. However there are some organic compounds which despite being essential for a healthy diet cannot be made by cells so must be provided by diet. These are essential amino acids, essential fatty acids and vitamins. Carbohydrates. Carbohydrates are a rapid source of energy, they are the body's fuel. The bulk of a balanced diet should be made from carbohydrates. A Balanced Diet Show me 'post it' By the end of this lesson. On a 'post it' note write down everything you have learned during today's lesson. A balanced diet is important because your organs and tissues need proper nutrition to work effectively. NOTE: Healthline isn't a healthcare provider. The ideal diet for an athlete is not very different from the diet recommended for any healthy person. However, the amount of each food group you need will depend on. ![]() Answer Selected Answer 30 Correct Answer Evaluation Method Exact. Note: Please write your answers. How to Maintain a Balanced Diet. After you write up your. ![]() ![]() ![]() How to Write a Nutrition Plan. Make a note of your total allowed fat grams for the day to remind you to choose low. Balanced Meals for a Healthy Diet. ![]() Hills Prescription Diet ? It’s common sense to conclude that a well fed dog is a happier and healthier dog. Using a combination of balanced nutrition plus vitamin supplements targeted toward specific symptoms and problems, it’s been proven that dogs and cats feel better, live longer and require less medication over the course of their lifespan. Hill’s Prescription Diet I/D Digestive Care - Many pets suffer from inefficient digestion leading to stomach upset and regular vomiting. Another Study found that NSAIDS (non- steroidal anti- inflammatory drugs) can often be reduced when fed Hill’s Prescription Diet J/D Joint Care. HILL’S LOVE OF PETSThe Hill's Food, Shelter & Love. Join us in giving these pets a loving home. ![]() ![]() Amazon.com: Hill's Science Diet Adult Advanced Fitness Chicken & Barley Recipe Dry Dog Food, 38.5-Pound Bag: Pet Supplies. ScienceDirect is the world's leading source for scientific, technical, and medical research. Explore journals, books and articles. Hill's Science Diet Puppy Healthy Development dog food provides precisely balanced, easy-to-digest nutrition for growing puppies. Discover the benefits of Hill's Science Diet dog and cat food: specially formulated for your pet's life stage, life care, and lifestyle needs. Check out how you can help your pet fight the effects of aging with New Hill Hills Science Diet Adult Perfect Weight Liver & Chicken Entree Canned Cat Food $26.16 $21.74 save 17% compare. More options available Hill's Science Diet. Free 1-2 day shipping at $49+, great prices & 365-day return policy. Buy Hill's Science Diet Id Dog Food at Wag.com. ![]() ![]() ![]() I Just Started Exercising . You plan to run a 5. K or marathon. You want to enhance your fitness for. Advertising on our site helps support our mission. We do not endorse non- Cleveland Clinic products or services. ![]() The pounds won’t hang around if you keep at it.“The key point here is that weight and muscle mass changes will occur. This causes small micro tears, also known as micro trauma, and some inflammation. Those two conditions in your muscle fibers are the reason you may gain some weight. Your body responds to the micro tears and inflammation in two ways that cause temporary water weight gain. The first is a healing response. Eat properly and give your muscles the proper amount of rest so they can. Calabrese says. RELATED. That water adds a small amount of weight, too. But this won’t happen right away. It will take you at least a month or two to add any lean muscle mass that would show up in your weight. By that point, you will probably be experiencing a good weight- loss trend because of the exercise. He or she can help you map out your exercise program, learn about the proper nutrition and rest you will need, and discuss the. ![]() ![]() ![]() ![]() Why Am I Gaining Weight If I'm Working Out? Muscle grows at a rate of about. Why Am I Gaining Weight? Dieting But Still Gaining Weight? By Everyday Health Editors. As you start to exercise more and eat a healthier diet. Lay out your diet and training plans. Your weight training needs to be infrequent but intense. Diet & Weight Management. Eating to Lose Weight and Build Muscle: How the NFL Does It. If you're working out three days a week. Sign Out; Weight Gain Home. Surprising Reasons You're. Wiki How to Gain Weight and Muscle. Gaining weight faster than this or using unhealthy foods to help you. Although working out regularly is essential to. Exercising but Gaining Weight. Wondering 'why am I gaining weight while working out?'. ![]() ![]() You're gaining muscle faster than you're losing fat. ![]() ![]() ![]() ![]() Diet composition of sailfish (Istiophorus platypterus) from the southern Gulf of California, Mexico. Diet composition of the sailfish Istiophorus platypterus from the southern Gulf of California was determined using stomach contents of 5. They were sampled from 1. Mexican Pacific (La Paz, Cabo San Lucas, Mazatlan, Puerto Vallarta, Barra de Navidad, and Manzanillo). A total of 7. 8 different prey taxa was classified and 6. From the diet composition and using the percent of index of relative importance (IRI), three feeding zones were determined by using cluster analysis. The most important prey by zones were in Zone I, La Paz: Dosidicus gigas, Scomber japonicus, and Auxis spp.; Zone II, Cabo San Lucas: Auxis spp., Selar crumenophthalmus, and Lagocephalus lagocephalus; and Zone III, Mazatlan, Puerto Vallarta, Barra de Navidad, and Manzanillo: Argonauta spp., D. We suggest that sailfish in Mexican Pacific waters are generalist predators feeding mainly on epipelagic species in coastal and oceanic waters, and occasionally diving to prey on demersal fish. The changes in diet composition among zones seem to be related more to abundance and distribution of the prey than to food preferences. ![]() ![]() ![]() Size: Pacific sailfish. Atlantic sailfish (Istiophorus albicans) and Indo-Pacific sailfish. Fact sheet: sailfish Author: Christine. Fish Profile for Indo-Pacific sailfish. Advertise on Aquafind. Shrimp & Seafood Recipes. ![]() Indo-Pacific sailfish. Found in the Indo-West Pacific. Indo-Pacific sailfish : Istiophorus platypterus : Indian and Pacific. Diet of four tuna species of The Western and Central Pacific Ocean. Feeding and Diet The Sailfish is an oceanic species that feeds on schooling. Kids' Inquiry of Diverse Species. Primary Diet; carnivore. Indo-Pacific sailfish are frequently caught by the nets of commercial tuna. Sailfish <em>Istiophorus platypterus</em> The two main subspecies of sailfish, Atlantic and Indo-Pacific. Indo-Pacific sailfish, or just sailfish. Their diet also includes faster fish like tuna and mackerel, made possible because of their own fast swimming. ![]() ![]() Treatment for hypertension includes diet and exercise. Common drug classes prescribed to treat hypertension are beta. Hypertension have blood pressure < 140/90. DASH diet Weight loss if. Beta antagonist (CHF, ASCVD, AV node. Beta blocker, also written . A 2007 study revealed diuretics and beta blockers used for hypertension. Beta-Blockers for High Blood Pressure. Generic Name Brand Name; acebutolol: Sectral: atenolol. Hypertension DASH Diet; A Visual Guide to. Beta blockers - Mayo Clinic. Reprint Permissions. A single copy of these materials may be reprinted for noncommercial personal use only. Atenolol is a beta-adrenergic antagonist indicated for management of hypertension. Clients are not usually placed on a 2-g sodium diet for hypertension.![]() Hypertension - beta-blockers lower blood. Mediterranean diet enriched with virgin. Hypertension and diabetes mellitus are common diseases in the United States. Patients with diabetes have a much higher rate of hypertension than would be. Beta blockers, also called beta-adrenergic blocking agents, treat a variety of conditions, such as high blood pressure and migraines. Adrenergic Pharmacology. 5) Beta blockers are also useful in. Read medical definition of Beta-agonist. Beta-agonists can be administered by inhalers or orally. ![]() ![]() Causes of the disease Diet and lifestyle are major factors thought to influence susceptibility to many diseases. Drug abuse, tobacco smoking, and alcohol drinking, as well as a lack of or too much exercise may also increase the risk. Lactose intolerance is frequently a side effect of celiac disease. Celiacs who eat gluten become lactose intolerant after the villi and microvilli in their small intestine become damaged, and are no longer capable of. Such rejected or condemned animals shall at once be removed by the owners from the pens containing animals which have been inspected and found to be free from disease and fit for human food, and shall be disposed of in. Learn about Crohn's disease and the causes, symptoms (including abdominal pain, diarrhea, weight loss, fever, rectal bleeding, and more) and treatment including diet, of this chronic inflammatory disease of the intestines. Alcohol-related neurologic disease is caused by excessive consumption of alcohol. When you consume alcohol, it is absorbed into your bloodstream from the stomach and the small intestine. It is then broken down by the. A study of ancient bodies has determined that cancer is a man-made disease, one fueled by the excesses. Tumors turn out to be extremely rare until very recent times, when pollution and poor diet became issues. Alcohol- Related Neurologic Disease: Definition and Patient Education What is alcohol- related neurologic disease? Alcohol- related neurologic disease is a range. Alcohol is often consumed as a social. Drinking too much alcohol. In particular, alcohol has a significant. Aside from intoxication, or drunkenness. Long- term abuse can damage the nervous. This damage may be irreversible. Drinking too. much alcohol can also alter levels of certain nutrients in your body. B- 1folate, or vitamin B- 9vitamins B- 6 and B- 1. These vitamins are needed for proper nerve. A poor diet can make problems even worse. Alcohol- related neurologic disease includes. Women are more susceptible than men to many. Moderate drinking is probably safe for most. But the best way to prevent alcohol- related neurologic disease is to. What are the types of alcohol- related neurologic disease and their symptoms? Alcohol abuse can have many direct and. Examples of neurologic. Wernicke- Korsakoff disease (WKS)This condition is caused by brain damage due. B1, deficiency. Thiamine deficiency is common in. There are two different WKS syndromes: Wernicke’s encephalopathy is severe and short- lived. ![]() Symptoms include: mental confusionpoor muscle coordinationparalysis of the nerves that move the. Korsakoff psychosis is long- lasting, or chronic. It usually develops as Wernicke's. Symptoms may include: problems with learning and memory. Alcoholic. neuropathy. This condition occurs when the peripheral. This can be permanent. Deficiencies in. B- 6 and B- 1. E can make it worse. These. vitamins are all needed for proper nerve function. ![]() ![]() ![]() ![]() Symptoms include: numbness, tingling, and prickly sensations in the arms and legsmuscle spasms and crampsmuscle weaknessmovement disordersurinary and bowel problems like incontinence, constipation, and. Alcohol withdrawal syndrome. ![]() Alcohol withdrawal syndrome occurs when. Symptoms can develop just five hours. Common symptoms include: anxietydepressionfatiguemood swingsshakinessnightmaresheadachesweatingnausea and vomitinginsomnia. ![]() A more serious version of withdrawal is. This can. cause: confusionsudden mood changeshallucinationsfeverhyperthermiaseizures. These symptoms can occur in addition to the. Alcoholic cerebellar degeneration. This condition occurs when neurons in the. The. cerebellum is the part of the brain that controls coordination and balance. Drinking too much alcohol over time can weaken the muscles. Symptoms include: muscle weaknessatrophy (decrease in muscle mass, also called muscle wasting)muscle crampsstiffnessspasms. Fetal. alcohol syndrome. Fetal alcohol syndrome occurs when a woman. Risks for the baby include brain damage. These issues can appear at. No amount of alcohol is safe to drink while. What causes alcohol- related neurologic disease? Alcohol- related neurologic disease is caused. When you consume alcohol, it is absorbed. It is then. broken down by the liver and expelled from the body. The liver can only break down alcohol in. The alcohol will continue to circulate in the. Symptoms of Parathyroid Disease (Hyperparathyroidism) Loss of energy. Don't feel like doing much. Hard to explain but just feel kind. Liver Disease: Signs, Symptoms, and Diagnosis Column written by: Dr. Fleming, Sherwood Animal Clinic (Regina, Saskatchewan, Canada) This topic is as big as the. All of the articles on this site are the intellectual property of the. Alcohol can have significant negative effects. CNS). Consumption also has negative. PNS). This includes the nerves that send. How alcohol affects the brain and nervous. How is alcohol- related neurologic disease diagnosed? Early diagnosis is important to prevent permanent. Your doctor will take a thorough health history and have. It is important that you fill out. Diagnosis depends. These may include: neglecting major responsibilities at work, school, or at homedrinking while drivingarrests for driving drunk or fighting while drunkinability to limit drinkingcontinued use of alcohol despite negative consequences. Some tests can be performed by your doctor to. The earlier you stop intake, the more likely. You may need inpatient rehab, especially if you exhibit alcoholism. A good source of help is support from family and. Other support sources include: local Alcoholics Anonymous (AA). Once you stop alcohol intake, a doctor can. Every person’s needs are different. Doctors. tailor specific treatments and alcohol abstinence programs to the individual. Treatment may include: vitamins and supplementsphysical therapyprescription medicationpainkillers. Intravenous thiamine may reverse the symptoms. WKS. But delirium tremens is a medical emergency and requires a hospital. You may need to be sedated for more than a week until the alcohol. And a doctor may use brain- imaging techniques to. What can you expect long- term? Your condition can get worse if you continue. Permanent damage to the nervous system and other parts of the. This may lead to: disabilitychronic paindeath. Completely avoiding alcohol and eating a. And a full recovery is possible. Your chances. depend on how early the disease is diagnosed and how much damage has already. It also depends on how motivated you are to. According to the National Institute on Alcohol Abuse and Alcoholism, most people who misuse alcohol and have mental damage show some. For. others, improvement may take longer. How can alcohol- related neurologic disease be prevented? Early intervention by doctors or family and. Steps you can take for prevention include: educating yourself on how much. Ultimately, the best way to prevent. SGK, renal function and Hypertension - Europe PMC Article. J Nephrol. Author manuscript; available in PMC 2. May 1. 9. Published in final edited form as: J Nephrol. Nov- Dec; 2. 3(0 1. S1. 24. PMCID: PMC4. NIHMSID: NIHMS5. 76. Department of Physiology, University of Tuebingen, Germany. Department of Pharmacology, University of Tuebingen, Germany. How much fat should you eat on a ketogenic diet? Are you following a ketogenic diet for weight maintenance or weight loss? Depending on the reason, you.Departments of Medicine and Pharmacology, University of California San Diego, VA San Diego Healthcare System, San Diego, USACorresponding author: Florian Lang, Dept. It is activated by insulin and growth factors via phosphatidylinositol- 3- kinase and the 3- phosphoinositide dependent kinase PDK1. SGK1 enhances the activity of a variety of ion channels, such as ENa. C, TRPV5, ROMK, KCNE1/KCNQ1 and Cl. CKb, carriers, such as NHE3, NKCC2, NCC and SGLT1, as well as the Na+/K+- ATPase. SGK1 contributes to Na+ retention and K+ elimination of the kidney as well as mineralocorticoid stimulation of salt appetite. A certain SGK1 gene variant (combined polymorphisms in intron 6 . The SGK1 gene variant has been shown to affect 3–5 % of Caucasians and some 1. Africans. The gene variant sensitizes the carriers to the hypertensive effects of hyperinsulinemia. Moreover, the SGK1 gene variant is associated with increased body mass index, presumably a result of enhanced SGLT1 activity with accelerated intestinal glucose absorption. Obesity predisposes the carriers of the gene variant to development of type II diabetes. Moreover, SGK1 stimulates coagulation. Thus, SGK1 may participate in the pathogenesis of metabolic syndrome or syndrome X, a condition characterized by the coincidence of essential hypertension, procoagulant state, obesity, insulin resistance and hyperinsulinemia. Keywords: blood pressure, obesity, fibrosis, inflammation, coagulation. Introduction. The serum- and glucocorticoid- inducible kinase 1 (SGK1) was originally cloned as an immediate early gene transcriptionally stimulated by serum and glucocorticoids in rat mammary tumor cells (1). The human isoform has been discovered as a gene upregulated by cell shrinkage (2). Compelling evidence points to a significant role of SGK1 in the pathophysiology of hypertension. The present brief review thus describes the physiological and pathophysiological impact of SGK1. Due to limited space, the citations had to be restricted and the reader may study a more comprehensive review (3) for more detailed information and earlier publications. Regulation of SGK1 transcription and activity. As reviewed elsewhere (3, 4), SGK1 transcription is stimulated by a wide variety of factors (4) including glucocorticoids, mineralocorticoids. D3 (1,2. 5(OH)2. D3), transforming growth factor . Distinct translational SGK1 isoforms differ in regulation of expression, subcellular localization and function (3, 4). Sgk: an old enzyme revisited. Hyperaldosteronism due to a low-salt diet may induce other forms of Sgk. You have full text access to this OnlineOpen article mTORC2-SGK-1 acts in two environmentally responsive pathways with opposing effects on longevity. SGK1 is expressed in a wide variety of organs (3) including the kidney. The subcellular localisation of SGK1 presumably depends on the functional state. Cellular exposure to serum triggers importin- alpha mediated entry of SGK1 into the nucleus (3) whereas activation by hyperosmotic shock or glucocorticoids increases the cytosolic fraction of the kinase (1). SGK1 has further been localized to the mitochondrial membrane (3, 4). Expressed SGK1 is activated by the phosphatidylinositol- 3- kinase (PI3- kinase) pathway involving 3- phosphoinositide (PIP3)- dependent kinase PDK1 and the mammalian target of rapamycin complex 2 TORC2, as well as the serine/threonine kinase WNK1 (with no lysine kinase 1) (3, 4). The PI3- kinase pathway and thus SGK1 is activated by insulin and several growth factors including IGF1 and hepatic growth factor (HGF) (3). Signaling involved in activation of SGK1 further includes bone marrow kinase/extracellular signal- regulated kinase 5 (BK/ERK5) or p. ![]() SGK1 is ubiquitinated by the ubiquitin ligase Nedd. Molecular targets of SGK1. SGK1 and related kinases (3) phosphorylate target proteins at the consensus sequence R- X- R- X- X- (S/T)- phi (X = any amino acid, R = arginine, phi = hydrophobic amino acid). The only exclusive targets of SGK1 thus far identified are the N- myc downregulated genes NDRG1 and NDRG2 (3, 4). SGK1 regulates a wide variety of channels, including the renal epithelial Na+ channel ENa. C (Fig. 1), the renal outer medullary K+ channel ROMK1, the Ca. Cell Surface Expression of the ROMK (Kir 1.1) Channel Is Regulated by the Aldosterone-induced Kinase, SGK-1, and Protein Kinase A*. Proteinuria in mice expressing PKB/SGK-resistant GSK3. SGK, renal function and. TRPV5,6, the Cl. SGK1 stimulates the Na. Cl cotransporter NCC, the Na+,K+,2. Cl. 1), GLUT1, GLUT4, the amino acid transporters ASCT2, SN1, EAAT1, EAAT2, EAAT3, EAAT4, EAAT5, the peptide transporters Pep. T1/2, the Na+, dicarboxylate cotransporter Na. DC- 1, the creatine transporter Crea. T, the Na+, myoinositol cotransporter SMIT, the phosphate transporter Na. Pi. IIb, and the Na+/K+- ATPase (3, 4, 7–9). Role of SGK1 in the stimulation of renal epithelial Na+ channel ENa. C by aldosterone and intestinal glucose transporter SGLT1 by glucocorticoids. SGK1 regulates channels and carriers in part by direct phosphorylation of the target proteins (3). SGK1 further phosphorylates the ubiquitin ligase Nedd. Phosphorylated Nedd. SGK1 further phosphorylates WNK4, a kinase inhibiting ENa. C activity (3, 4). SGK1 inhibits inducible nitric oxide synthase, thus abrogating the inhibitory effect of NO on ENa. C (3, 4). SGK1 is further effective through activation of the phosphatidylinositol- 3- phosphate- 5- kinase PIKfyve and subsequent formation of PIP2 (3, 4). SGK1 may also influence channel or carrier expression (3, 4). The SGK1 dependent regulation of ENa. C is in part due to impaired SGK1- mediated phosphorylation of Af. ENa. C. SGK1 participates in the regulation of salt intake (1. Accordingly, mineralocorticoids stimulate salt intake in sgk. SGK1 participates in the pathophysiology of metabolic syndrome (see below), allergy, pulmonary hypertension, cardiac hypertrophy, tumor growth and metastasis as well as inflammation and fibrosis (3, 4). SGK1 dependent regulation of renal function. SGK1 contributes to the stimulation of renal Na+ excretion by aldosterone, insulin and IGF1 (3, 4, 1. Part of the effect of aldosterone on ENa. C is independent of SGK1 and effects of aldosterone and SGK1 are in part additive. In contrast, the effects of antidiuretic hormone (ADH) or insulin are fully dependent on SGK1 (1. In SGK1- knockout (sgk. The renal salt loss of sgk. The hyperaldosteronism in sgk. Similarly, despite the lack of SGK1 the colonic ENa. C activity is enhanced in sgk. Inhibition of ENa. C by triamterene leads to eventually lethal salt loss in sgk. The presence of SGK1 is a prerequisite for the antinatriuretic effect of insulin, which is significantly blunted in sgk. The anticalciuria is presumably the result of extracellular volume contraction following renal salt loss due to impaired stimulation of Na. Cl cotransport and ENa. C (3). The volume contraction enhances proximal tubular Na+ and Ca. Ca. 2+ excretion. Pharmacological inhibition of Na. Cl cotransport by thiazide diuretics similarly lead to anticalciuria (2. Ca. 2+ reabsorption (2. Proximal tubular SGK1 expression is low in normal kidneys (3) and SGK1 presumably does not participate in the regulation of proximal tubular transport. Hyperglycemia, however, enhances proximal tubular expression of SGK1, which in turn stimulates renal tubular glucose transport (2. SGK1 expression in glomerular podocytes (2. The proteinuria following DOCA treatment is significantly blunted in SGK1 knockout mice (2. SGK1- dependent renal salt retention contributes to the development of edema during treatment with PPAR. Moreover, enhanced SGK1 expression was found during ascites formation in cirrhotic rats (2. SGK1 sensitive hypertension and metabolic syndrome. Owing to its influence on renal salt excretion and salt intake SGK1 is expected to participate in blood pressure control. Hyperinsulinemia by pretreatment with a high- fructose diet (1. In accordance, the antinatriuretic effect of insulin observed in sgk. Moreover, SGK1 plays a critical role in the hypertensive effects of glucocorticoids (3. In humans a certain variant of the SGK1 gene (the combined presence of distinct polymorphisms in intron 6 . The gene variant affects some 3–5 % of Caucasians (3) and some 1. Africans (3. 1). The gene variant is particularly associated with insulin- sensitivity of blood pressure increase (3. The same SGK1 gene variant is associated with increased body mass index (3). Accordingly, the SGK1 gene variant is more prevalent in patients with type 2 diabetes than in individuals without family history of diabetes (3. The impact of SGK1 on body weight results presumably from the stimulating effect of SGK1 on intestinal glucose absorption, which predisposes to obesity (3). Hypertension, obesity and susceptibility to develop type II diabetes are hallmarks of metabolic syndrome, a condition associated with enhanced morbidity and mortality from cardiovascular disease (3). Metabolic syndrome is associated with enhanced coagulation (3), which is again stimulated by SGK1 (3. Accordingly, SGK1 presumably participates in the pathophysiology of metabolic syndrome. Moreover, maternal SGK1 contributes to fetal programming of hypertension (Fig 2). Protein deficient diet during pregnancy leads to increased blood pressure in offspring only, if the mother expresses SGK1 (3. Role of maternal SGK1 in fetal programming of blood pressure. Conclusions. SGK1 participates in the regulation of renal tubular Na+ reabsorption and intestinal glucose absorption. The kinase thus contributes to blood pressure and body weight control. Accordingly, deranged SGK1 activity could lead to metabolic syndrome. Footnotes. Disclosure: The study in the laboratories of the authors is funded by the Deutsche Forschungsgemeinschaft (DFG to F. L.) and National Institutes of Health (NIH- RO1. HL, Paul, Roland, NIH- R0. DK5. 62. 48 and NIH- P3. DK0. 79. 33. 7 to V. V.). The authors declare that they have no conflict of interest and has been seen and approved by all authors and that it is not under consideration for publication elsewhere. References. 1. Firestone GL, Giampaolo JR, O’Keeffe BA. SGK - Science. Direct Topics. Steroid Hormones such as Aldosterone Bind to Cytoplasmic Receptors and Regulate Nuclear Transcription Events Aldosterone is a steroid hormone that binds to and activates the ineralocorticoid eceptor (MR), which is present in the principal cell, but also in other cell types including intestinal epithelial cells, neuronal cells, and cardiac myocytes. The MR is a member of the steroid/thyroid family of ligand- inducible transcription factors that includes the vitamin D receptor, glucocorticoid receptor, thyroid receptor, and retinoic acid receptor (reviewed in 2. Unlike the transmembrane receptors discussed in the section . The ligand, such as thyroid hormone or aldosterone, can cross the cell membrane, bind the cytosolic receptor, and then translocate as a ligand. In the case of aldosterone, these regulatory sequences are found in the promoter regions of target genes such as SCNN1. A (the ENa. C . In the principal cell, the . The increase in ENa. C . In this manner, aldosterone directly increases the total number of active ENa. C transporters available in the cell, leading to an increase in sodium reabsorptive capacity. A second way in which aldosterone can increase the number of ENa. C channels available to reabsorb sodium is by inhibiting ENa. C degradation. This is mediated by the transcriptional regulation of SGK expression. SGK is a serine- threonine kinase that phosphorylates and inactivates Nedd. At the membrane, the ubiquitin ligase Nedd. ENa. C, targeting it for internalization and proteosomal degradation. Nedd. 4- 2 function is inhibited following phosphorylation by SGK, further increasing ENa. C expression at the cell membrane, and therefore sodium reabsorptive capacity. Vasopressin (AVP), acting through the V2 GPCR, can also increase collecting duct sodium reabsorption. V2 activation leads to c. AMP production and subsequent PKA activation. Like SGK, PKA can phosphorylate and inhibit Nedd. By increasing SGK expression, aldosterone inhibits Nedd. ENa. C degradation, and thereby increases the amount of ENa. C present on the cell surface. Mutations in ENa. C that prevent its association with Nedd. ENa. C expression, resulting in the progressive hypertension seen in Liddle. For membrane channels this typically means a change in the open probability (P) of the channel (the time that the channel spends in the open configuration). ROMK (also known as Kir. TAL, and potassium secretion in the collecting duct (reviewed in 2. One of the major determinants of P for ROMK is the concentration of PIP in the membrane in the vicinity of the channel, an effect that appears to be due to an extensive series of interactions between the basic amino acids in the carboxy terminus of ROMK and the negatively charged head groups of the membrane phospholipids (reviewed in 2. PIP is produced by lipid kinases such as the PI(4)P kinase, and degraded by phospholipases such as PLA and PLC (reviewed in 2. Thus, it is speculated that signals that enhance PIP production or inhibit its degradation will increase ROMK activity at the membrane, whereas pathways that reduce PIP levels, such as activation of PKC, will inhibit its activity. Alterations in the P for ROMK have also been found to be due to direct phosphorylation of the channel by PKA (reviewed in 2. In vitro studies have demonstrated three PKAphosphorylation sites in ROMK, and phosphorylation of two of those sites (serine 2. P for the channel, without changing the number of channels at the membrane. As with other PKA effectors, the presence of the appropriate AKAP is required to target activated PKA to ROMK at the membrane. Although the precise mechanism by which PKA phosphorylation regulates P in ROMK has yet to be determined, it appears that at least part of the effect is due to an increased affinity of ROMK for PIP, thus reducing the concentration of PIP needed to support the channel in the open state. Based on these studies, it is presently believed that the AVP- stimulated increase in thick ascending limb potassium recycling is due to V2- dependent activation of PKA, and subsequent phosphorylation and activation of ROMK. Similar to the regulation of aquaporin- 2 and ENa. C, ROMK can also be regulated by altering channel location or synthesis. Several kinases have been implicated in regulating the trafficking of ROMK, including PKA, SGK, and a recently described kinase WNK (ith o (lysine)). As noted above, there are three PKAphosphorylation sites on ROMK. While two of the sites directly regulate channel open probability, phosphorylation of the third residue (serine 4. In addition to PKA, SGK can phosphorylate ROMK on serine 4. This appears to occur in concert with a scaffolding protein, NHERF2, which increases trafficking of ROMK to the membrane via its interaction with the carboxy terminal PDZ- binding motif. Thus, the increased expression of SGK following aldosterone stimulation can lead to sustained increases in ROMK- dependent potassiumexcretion via increased numbers of channels on the cell membrane. Recently, another family of serine/threonine kinases, the WNKs, have been found to play an important role in regulating the activity of diverse ion channels in the kidney (reviewed in 2. To date there have been four WNK kinases described in humans, all sharing the unusual substitution of a cysteine residue for the more typical lysine in . Mutations of WNK1 and WNK4 have been shown to cause pseudohypoaldosteronism II (PHAII), a syndrome consisting of hypertension with increased sodium reabsorption and hyperkalemia. The mechanisms by which WNKs regulate ROMK and NCC depend on distinct aspects of WNK function. Mutations in WNK1 and WNK4 that cause PHAII result in decreased ROMK at the membrane, and therefore hyperkalemia due to decreased K secretion. It has been shown that ROMK associates with a complex including WNK1, WNK4, and the scaffolding protein intersectin, and that intersectin is required for the endocytosis of ROMK in clathrin- coated vesicles. The formation of this complex is independent of WNK kinase activity, and instead requires the association of proline- rich regions of WNK1 and WNK4 with the SH3 domain of intersectin. Mutations in WNK4 that cause PHAII appear to increase the association of the ROMK. This process is complex and not yet fully elucidated, but appears to involve a balance between WNK4- dependent degradation of NCC and WNK1- dependent activation of NCC that is present on the cell surface (reviewed in 2. In the presence of active WNK4, newly synthesized NCC is targeted via sortilin for lysosomal degradation rather than cell surface expression, thus reducing the pool of NCC available for sodium transport. In contrast, WNK1 and WNK3 activate the sodium transport function of NCC that is on the cell surface by phosphorylating the intracellular kinase SPAK, which then phosphorylates and activates NCC. A second phosphorylation target of WNK3 is WNK4 itself, resulting in inhibition of the WNK4- mediated NCC degradation, and thus increasing NCC surface expression. Mutations in WNK4 that cause PHAII result in increased sodium reabsorption at least in part due to increased NCC on the cell surface. |
AuthorWrite something about yourself. No need to be fancy, just an overview. Archives
November 2017
Categories |