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Type 1 Diabetes Metabolism

Protein And Energy Metabolism In Type 1 Diabetes

Protein And Energy Metabolism In Type 1 Diabetes

Protein and Energy Metabolism in Type 1 Diabetes We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Protein and Energy Metabolism in Type 1 Diabetes Profound metabolic changes occur in people with type 1 diabetes mellitus during insulin deprivation. These include an increase in basal energy expenditure and reduced mitochondrial function. In addition, protein metabolism is significantly affected during insulin deprivation. A greater increase in whole-body protein breakdown than protein synthesis occurs resulting in a net protein loss. During insulin deprivation the splanchnic bed has a net protein accretion which accounts for the total increase in whole-body protein synthesis while muscle is in a net catabolic state. Keywords: energy metabolism, insulin, mitochondria, protein synthesis, type 1 diabetes In the absence of insulin replacement type 1 diabetes is a catabolic condition with severe depletion of both energy stores and protein mass. Since most type 1 diabetic individuals are treated with insulin, a short period of insulin withdrawal in these individuals provides a model system to study the role of insulin in energy and protein metabolism. The causes of negative energy balance and protein catabolism have been extensively studied in people with type 1 diabetes and will be reviewed in this article. Profound changes in energy metabolism occur in people with type 1 diabetes mellitus (T1DM) during insulin deprivation in addition t Continue reading >>

Metabolism And Diabetes

Metabolism And Diabetes

Home - Science - Research - Metabolism and Diabetes Humans are built to hunger for fat, packing it on during times of feast and burning it during periods of famine. But deluged by foods rich in fat and sugar, the modern waistline often far exceeds the need to store energy for lean times. The result has been an epidemic of metabolic diseases. At Salk, we are deciphering the blueprint for metabolism, the complicated biological system that evolved to store and burn food for energy. These blueprints allow us to identify the molecular and genetic causes of obesity, diabetes and other metabolism-related disorders. Were developing the next generation of obesity and diabetes therapies. We know that whats needed now are powerful cures to fight a growing epidemic. Individuals with type 1 diabetes cannot regulate their blood sugar levels because their pancreas does not produce enough insulin. There is no cure for this disease, which is diagnosed in about 40,000 people annually in the United States. It can be managed, but there are still risks for serious complications, including blindness, heart attack, kidney failure and stroke. At the Salk Institute, we are focusing on the islet cells in the pancreas, which are responsible for producing insulin. We are looking for ways to protect them from damage or to coax them back to health. Our regenerative medicine research on stem cells is currently paving the way to grow new pancreatic tissues in the lab, healthy tissues that can benefit those people with type 1 diabetes. Were doing the science today so that one day people wont have to live with this disease. Continue reading >>

Diabetes And Sugar Metabolism

Diabetes And Sugar Metabolism

Sugar metabolism is the process of turning the energy from the foods you eat into fuel your body's cells need to grow and function. If you have diabetes, you have a problem with insulin, which is an important hormone in sugar metabolism. Sugar Metabolism: From Food to Fuel When you eat foods, enzymes in the digestive process break down proteins, fats, and carbohydrates into amino acids, fatty acids, and simple sugars. These byproducts are absorbed into your blood, where they are available to be used as energy when your body needs it. The most important source of fuel for your body is a simple sugar called glucose, also known as blood sugar, which builds up in your blood after a meal. Blood sugar can then travel throughout your bloodstream to be used by cells throughout your body. Your pancreas, a gland located behind your stomach, is in control of releasing hormones that tell your body whether to store or release energy for your body to use. One of these hormones, insulin, is essential for helping your body use blood sugar and preventing a build-up of blood sugar in your bloodstream. Insulin “unlocks” your cells to allow the sugar circulating in the blood to enter the cells where it can be turned into energy. After you have eaten a meal, your pancreas senses a rise in your blood sugar level and releases the precise amount of insulin needed to move sugar from your blood into your cells. How Diabetes Affects Sugar Metabolism If you have diabetes, your body has problems producing insulin, responding to insulin, or both. When insulin is not working as it should, blood sugar can build up, eventually spilling over into your urine. This can lead to diabetes symptoms such as increased urination and unexplained weight loss, since your body isn't able to use the energy from t Continue reading >>

Diabetes Mellitus Type 1

Diabetes Mellitus Type 1

Diabetes mellitus type 1 (also known as type 1 diabetes) is a form of diabetes mellitus in which not enough insulin is produced.[4] This results in high blood sugar levels in the body.[1] The classical symptoms are frequent urination, increased thirst, increased hunger, and weight loss.[4] Additional symptoms may include blurry vision, feeling tired, and poor healing.[2] Symptoms typically develop over a short period of time.[1] The cause of type 1 diabetes is unknown.[4] However, it is believed to involve a combination of genetic and environmental factors.[1] Risk factors include having a family member with the condition.[5] The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas.[2] Diabetes is diagnosed by testing the level of sugar or A1C in the blood.[5][7] Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.[5] There is no known way to prevent type 1 diabetes.[4] Treatment with insulin is required for survival.[1] Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump.[9] A diabetic diet and exercise are an important part of management.[2] Untreated, diabetes can cause many complications.[4] Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma.[5] Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes.[4] Furthermore, complications may arise from low blood sugar caused by excessive dosing of insulin.[5] Type 1 diabetes makes up an estimated 5–10% of all diabetes cases.[8] The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year.[5] With Continue reading >>

Renal Amino Acid, Fat And Glucose Metabolism In Type 1 Diabetic And Non-diabetic Humans: Effects Of Acute Insulin Withdrawal

Renal Amino Acid, Fat And Glucose Metabolism In Type 1 Diabetic And Non-diabetic Humans: Effects Of Acute Insulin Withdrawal

, Volume 49, Issue8 , pp 19011908 | Cite as Renal amino acid, fat and glucose metabolism in type 1 diabetic and non-diabetic humans: effects of acute insulin withdrawal The aim of this study was to test the hypothesis that type 1 diabetes alters renal amino acid, glucose and fatty acid metabolism. We studied five C-peptide-negative, type 1 diabetic subjects during insulin replacement (glucose 5.6mmol/l) and insulin deprivation (glucose 15.5mmol/l) and compared them with six non-diabetic subjects. Leucine, phenylalanine, tyrosine, glucose and palmitate tracers were infused after an overnight fast and samples were obtained from the renal vein, femoral vein and femoral artery. Insulin deprivation significantly increased whole-body fluxes (2025%) of phenylalanine, tyrosine and leucine, and leucine oxidation (50%). Kidney contributed 510% to the whole-body leucine and phenylalanine flux. A net uptake of phenylalanine, conversion of phenylalanine to tyrosine (5mol/min) and net release of tyrosine (5mol/min) occurred across the kidney. Whole-body (three-fold) and leg (two-fold) leucine transamination increased but amino acid metabolism in the kidney did not alter with diabetes or insulin deprivation. Insulin deprivation doubled endogenous glucose production, renal glucose production was unaltered by insulin deprivation and diabetes (ranging between 100 and 140mol/min). Renal palmitate exchange was unaltered by insulin deprivation. In conclusion, kidney postabsorptively accounts for 510% of whole-body protein turnover, 1520% of leucine transamination and 1015% of endogenous glucose production, and actively converts phenylalanine to tyrosine. During insulin deprivation, leg becomes a major site for leucine transamination but insulin deprivation does not affect renal phenylalani Continue reading >>

Journal Of Diabetes & Metabolism

Journal Of Diabetes & Metabolism

The Journal of Diabetes & Metabolism is an open access publication that features scientific works of considerable significance and impact in all fields of Diabetes research such as: Type 1 Diabetes, Type 2 Diabetes, Gestational Diabetes, Monogenic Diabetes, and cystic fibrosis-related diabetes, Latent autoimmune diabetes of adults (LADA), Diabetic Neuropathy, Diabetic Retinopathy, Diabetic Nephropathy, Diabetic hypoglycemia, and Obesity. The scope of the journal is not just restricted to Diabetes alone; works related to endocrinology, genetics, physiology, or cardio-vascular diseases which are loosely associated with Diabetes are equally welcome. It is a boon for researchers and students who wish to be kept abreast of the latest advancements in the field of Diabetes, it would help them build on the current know-how. Business people, policy makers, journalists, and practitioners can also benefit from the works published in the journal. The journal is helmed by a highly accomplished editorial board which comprises of acclaimed scientists from all over the world. Each individual article is peer reviewed and approved for publication by eminent scientists in the field of Diabetology. The journal maintains the highest standards in terms of quality of content published. In addition to Research Articles, the Journal also publishes high quality Commentaries, Reviews, Perspectives, and Case Reports. The Journal of Diabetes & Metabolism aims to provide all the authors with an efficient, constructive, and courteous editorial process. The journal believes in expediting the publishing process; towards this end, the journal also provides advance posting of the accepted articles. This journal ensures the barrier-free distribution of its content on online and thus, helps in improving th Continue reading >>

Effects Of Type 1 Diabetes On Cells & Metabolism

Effects Of Type 1 Diabetes On Cells & Metabolism

Every year in the United States 13,000 children are diagnosed with type 1 diabetes, according to KidsHealth, a website published by the nonprofit Nemours Foundation. More than 1 million American children and adults will learn how to deal with the disease every day. Type 1 diabetes is a chronic condition for which there is no cure, but there are significant benefits to following treatment protocols designed to keep the disease under control. Video of the Day Type 1 Diabetes Type 1 diabetes was once called insulin-dependent diabetes or juvenile diabetes. Diabetes is a disease that ultimately affects how the body uses blood sugar. Blood sugar is derived from the food that we eat and is a necessary source of energy used to fuel all of your body functions. If you suffer from type 1 diabetes it is likely that your own immune system attacked and destroyed the cells in the pancreas that produce insulin. Insulin is required for cells to use blood sugar for fuel and energy. Type 1 diabetes cannot be prevented and there is no real way to predict who will get it, but scientists believe that there may be a genetic link in combination with an environmental factor, such as a virus. How Damage is Caused A high amount of blood sugar in the bloodstream is the cause of damage done at the cellular level. When these blood sugar levels rise beyond acceptable levels, the excess sugar can attach to proteins within the blood vessels, altering their normal structure and function. In this way the arterial blood vessels become thicker and less elastic, which makes it more difficult for blood to flow through. This reduction in arterial flow also reduces the amount of oxygen available to the tissues and can cause damage over time. Controlling blood sugar levels is the key factor to reducing the amou Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

Return to The Medical Biochemistry Page Diabetes is any disorder characterized by excessive urine excretion. The most common form of diabetes is diabetes mellitus, a metabolic disorder in which there is an inability to oxidize carbohydrate due to disturbances in insulin function. Diabetes mellitus is characterized by elevated glucose in the plasma and episodic ketoacidosis. Additional symptoms of diabetes mellitus include excessive thirst, glucosuria, polyuria, lipemia and hunger. If left untreated the disease can lead to fatal ketoacidosis. Other forms of diabetes include diabetes insipidus and brittle diabetes. Diabetes insipidus is the result of a deficiency of antidiuretic hormone (ADH, also referred to as vasopressin or arginine vasopressin, AVP). The major symptom of diabetes insipidus (excessive output of dilute urine) results from an inability of the kidneys to resorb water. Brittle diabetes is a form that is very difficult to control. It is characterized by unexplained oscillations between hypoglycemia and acidosis. Criteria, which clinically establish an individual as suffering from diabetes mellitus, include: 1. having a fasting plasma glucose level in excess of 126mg/dL (7mmol/L). Normal levels should be less than 100mg/dL (5.6mmol/L) or: 2. having plasma glucose levels in excess of 200mg/dL (11mmol/L) at two times points during an oral glucose tolerance test, OGTT, one of which must be within 2 hrs of ingestion of glucose. Different clinical labs may use different units for the measurement of serum glucose concentrations, either in mmol/L or mg/dL. One can easily interconvert these values using the following formulas: mg/dL x 0.0555 = mmol/L (or simply divide mg/dL by 18) mmol/L x 18.0182 = mg/dL (or simply multiply mmol/L by 18) The earlier a person is dia Continue reading >>

Intermediary Metabolism

Intermediary Metabolism

This page has yet to be adopted. If you would like to take it on please contact Anna Harding at [email protected] Insulin secretion starts to decline months or years before clinical onset of type 1 diabetes, and individuals studied prospectively often pass through a stage of impaired glucose tolerance before symptoms appear. Insulin deficiency leads to increased glucose output by the liver and reduced glucose uptake by peripheral insulin sensitive tissues such as muscle and fat. Blood glucose rises and spills into the urine, producing an osmotic diuresis. Insulin lack promotes fat breakdown, with release of triacylglycerol, non-esterified fatty acids (NEFA) and glycerol into the circulation. Protein breakdown is also accelerated, with release of amino acids into the circulation; amino acids such as alanine and other 3-carbon molecules such as glycerol provide the liver with further precursors for gluconeogenesis. The 'accelerated starvation' of uncontrolled diabetes results in overproduction of acidic ketone bodies in the hepatic mitochondria, and culminates in the metabolic emergency of diabetic ketoacidosis. Continue reading >>

Diabetes: Symptoms, Causes And Treatments

Diabetes: Symptoms, Causes And Treatments

Diabetes, often referred to by doctors as diabetes mellitus, describes a group of metabolic diseases in which the person has high blood glucose (blood sugar), either because insulin production is inadequate, or because the body's cells do not respond properly to insulin, or both. Patients with high blood sugar will typically experience polyuria (frequent urination), they will become increasingly thirsty (polydipsia) and hungry (polyphagia). Here are some key points about diabetes. More detail and supporting information is in the main article. Diabetes is a long-term condition that causes high blood sugar levels. In 2013 it was estimated that over 382 million people throughout the world had diabetes (Williams textbook of endocrinology). Type 1 Diabetes - the body does not produce insulin. Approximately 10% of all diabetes cases are type 1. Type 2 Diabetes - the body does not produce enough insulin for proper function. Approximately 90% of all cases of diabetes worldwide are of this type. Gestational Diabetes - this type affects females during pregnancy. The most common diabetes symptoms include frequent urination, intense thirst and hunger, weight gain, unusual weight loss, fatigue, cuts and bruises that do not heal, male sexual dysfunction, numbness and tingling in hands and feet. If you have Type 1 and follow a healthy eating plan, do adequate exercise, and take insulin, you can lead a normal life. Type 2 patients need to eat healthily, be physically active, and test their blood glucose. They may also need to take oral medication, and/or insulin to control blood glucose levels. As the risk of cardiovascular disease is much higher for a diabetic, it is crucial that blood pressure and cholesterol levels are monitored regularly. As smoking might have a serious effect on c Continue reading >>

Metabolic Syndrome And Type-1 Diabetes Mellitus: Prevalence And Associated Factors

Metabolic Syndrome And Type-1 Diabetes Mellitus: Prevalence And Associated Factors

Keywords Diabetes mellitus. Microvascular complications. Metabolic syndrome. Insulin resistance. Article INTRODUCTION Traditionally, persons with type-1 diabetes mellitus (DM1) usually have a normal or low weight and a tendency for the late development of arterial hypertension and dyslipidemia. Until a few years ago, the main causes of death in persons with DM1 were those derived from microvascular complications, particularly kidney disease.1 Although therapeutic advances for the treatment of DM1 and its main associated cardiovascular risk factors have led to significant reductions in the rates of death and microvascular complications,2-5 no similar trend has been seen with cardiovascular disease.6 Though DM1 involves the immune destruction of the pancreatic beta cells and usually presents at an early age, affected persons are not exempt from developing insulin resistance at some earlier stage in the course of the disease,7-9 which is known as "double diabetes." This phenomenon usually appears in patients with a family history of type 2 diabetes mellitus (DM2) and is associated with a greater body mass index, greater insulin requirements and worse metabolic control.10 As well as the insulin resistance, other factors can explain why cardiovascular disease is the leading cause of death in these patients, such as the chronic complications of DM1, like kidney disease,11 and the earlier age of onset of the disease, with the resulting longer period of exposure to the main cardiovascular risk factors, together with a poor control of these risk factors.12,13 As a consequence, the phenotypic characteristics and cardiovascular risk profile of patients with DM1 have become more similar to those of DM2 over recent years. Since the first description of the metabolic syndrome, by Rea Continue reading >>

Original Article Metabolic Syndrome In Type 1 Diabetes

Original Article Metabolic Syndrome In Type 1 Diabetes

Abstract Objectives The aim of this study was to assess the prevalence and effects of the presence of metabolic syndrome in patients with type 1 diabetes. Research design and methods Retrospective analysis of data from a one year period of patients attending annual review clinic was undertaken. Body weight, height and blood pressure were measured along with assessment of micro-/macro-vascular complications. HbA1c, urea, cholesterol, triglyceride, urinary albumin: creatinine ratios were also measured. Patients were divided into those with and those without metabolic syndrome. Results Data from 365 type 1 diabetic patients was analysed. Hundred and twelve had metabolic syndrome. There was no difference according to gender or smoking. Type 1 diabetic patients with metabolic syndrome had longer duration of diabetes, were significantly older, heavier, had higher blood pressure, higher triglyceride and lower HDL cholesterol levels. There were significant increases in mean BMI, urea, serum creatinine, urinary albumin: creatinine ratio, cholesterol and triglyceride in the group with metabolic syndrome even after controlling for both age and duration of diabetes. Neuropathy and macro-vascular complications were commoner in patients with metabolic syndrome. Patients with metabolic syndrome were more likely to be on statins, ACE inhibitors and angiotensin receptor blockers and had a significantly higher mean insulin dosage requirement per kg. Conclusions This study highlights the importance of the presence of the metabolic syndrome in patients with type 1 diabetes. It shows that metabolic syndrome is associated with a higher incidence of diabetes-related complications, a need for higher insulin doses and a more aggressive multifactorial intervention. Continue reading >>

Diabetes Mellitus (dm)

Diabetes Mellitus (dm)

Years of poorly controlled hyperglycemia lead to multiple, primarily vascular complications that affect small vessels (microvascular), large vessels (macrovascular), or both. (For additional detail, see Complications of Diabetes Mellitus.) Microvascular disease underlies 3 common and devastating manifestations of diabetes mellitus: Microvascular disease may also impair skin healing, so that even minor breaks in skin integrity can develop into deeper ulcers and easily become infected, particularly in the lower extremities. Intensive control of plasma glucose can prevent or delay many of these complications but may not reverse them once established. Macrovascular disease involves atherosclerosis of large vessels, which can lead to Immune dysfunction is another major complication and develops from the direct effects of hyperglycemia on cellular immunity. Patients with diabetes mellitus are particularly susceptible to bacterial and fungal infections. Continue reading >>

Lipid Metabolism And Its Implications For Type 1 Diabetes-associated Cardiomyopathy

Lipid Metabolism And Its Implications For Type 1 Diabetes-associated Cardiomyopathy

Lipid metabolism and its implications for type 1 diabetes-associated cardiomyopathy 1 Heart Failure Pharmacology, Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia 2 Central Clinical School, Monash University, Melbourne, Victoria, Australia 3 Lipid Metabolism & Cardiometabolic Disease Laboratory, Baker Heart & Diabetes Institute, Melbourne, Victoria, Australia 4 School of Biosciences, The University of Melbourne, Parkville, Victoria, Australia Correspondence should be addressed to R H Ritchie or A C Calkin; Email: [email protected] or [email protected] Diabetic cardiomyopathy was first defined over four decades ago. It was observed in small post-mortem studies of diabetic patients who suffered from concomitant heart failure despite the absence of hypertension, coronary disease or other likely causal factors, as well as in large population studies such as the Framingham Heart Study. Subsequent studies continue to demonstrate an increased incidence of heart failure in the setting of diabetes independent of established risk factors, suggesting direct effects of diabetes on the myocardium. Impairments in glucose metabolism and handling receive the majority of the blame. The role of concomitant impairments in lipid handling, particularly at the level of the myocardium, has however received much less attention. Cardiac lipid accumulation commonly occurs in the setting of type 2 diabetes and has been suggested to play a direct causal role in the development of cardiomyopathy and heart failure in a process termed as cardiac lipotoxicity. Excess lipids promote numerous pathological processes linked to the development of cardiomyopathy, including mitochondrial dysfunction and inflammation. Although somewhat underappreciated, cardiac lipotox Continue reading >>

Metabolic Syndrome In Type 1 Diabetes

Metabolic Syndrome In Type 1 Diabetes

Association with diabetic nephropathy and glycemic control (the FinnDiane study) Abstract OBJECTIVE—The aim of this study was to estimate the prevalence of the metabolic syndrome in Finnish type 1 diabetic patients and to assess whether it is associated with diabetic nephropathy or poor glycemic control. RESEARCH DESIGN AND METHODS—In all, 2,415 type 1 diabetic patients (51% men, mean age 37 years, duration of diabetes 22 years) participating in the nationwide, multicenter Finnish Diabetic Nephropathy (FinnDiane) study were included. Metabolic syndrome was defined according to the National Cholesterol Education Program diagnostic criteria. Patients were classified as having normal albumin excretion rate (AER) (n = 1,261), microalbuminuria (n = 326), macroalbuminuria (n = 383), or end-stage renal disease (ESRD) (n = 164). Glycemic control was classified as good (HbA1c <7.5%), intermediate (7.5–9.0%), or poor (>9.0%). Creatinine clearance was estimated with the Cockcroft-Gault formula. RESULTS—The overall prevalence of metabolic syndrome was 38% in men and 40% in women. The prevalence was 28% in those with normal AER, 44% in microalbuminuric patients, 62% in macroalbuminuric patients, and 68% in patients with ESRD (P < 0.001). Patients with metabolic syndrome had a 3.75-fold odds ratio for diabetic nephropathy (95% CI 2.89–4.85), and all of the separate components of the syndrome were independently associated with diabetic nephropathy. The prevalence of metabolic syndrome was 31% in patients with good glycemic control, 36% in patients with intermediate glycemic control, and 51% in patients with poor glycemic control (P < 0.001). Similarly, metabolic syndrome increased with worsening creatinine clearance. CONCLUSIONS—The metabolic syndrome is a frequent finding Continue reading >>

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