Topic
Insulin
About: Insulin is a research topic. Over the lifetime, 124295 publications have been published within this topic receiving 5129734 citations. The topic is also known as: human insulin.
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TL;DR: Recently, inexpensive quantitative tests of 3HB levels have become available for use with small blood samples (5–25 µl) and offer new options for monitoring and treating diabetes and other states characterized by the abnormal metabolism of ketone bodies.
Abstract: Ketone bodies are produced by the liver and used peripherally as an energy source when glucose is not readily available. The two main ketone bodies are acetoacetate (AcAc) and 3-beta-hydroxybutyrate (3HB), while acetone is the third, and least abundant, ketone body. Ketones are always present in the blood and their levels increase during fasting and prolonged exercise. They are also found in the blood of neonates and pregnant women. Diabetes is the most common pathological cause of elevated blood ketones. In diabetic ketoacidosis (DKA), high levels of ketones are produced in response to low insulin levels and high levels of counterregulatory hormones. In acute DKA, the ketone body ratio (3HB:AcAc) rises from normal (1:1) to as high as 10:1. In response to insulin therapy, 3HB levels commonly decrease long before AcAc levels. The frequently employed nitroprusside test only detects AcAc in blood and urine. This test is inconvenient, does not assess the best indicator of ketone body levels (3HB), provides only a semiquantitative assessment of ketone levels and is associated with false-positive results. Recently, inexpensive quantitative tests of 3HB levels have become available for use with small blood samples (5-25 microl). These tests offer new options for monitoring and treating diabetes and other states characterized by the abnormal metabolism of ketone bodies.
1,087 citations
TL;DR: An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin.
Abstract: Obesity has become a major worldwide health problem. In every single country in the world, the incidence of obesity is rising continuously and therefore, the associated morbidity, mortality and both medical and economical costs are expected to increase as well. The majority of these complications are related to co-morbid conditions that include coronary artery disease, hypertension, type 2 diabetes mellitus, respiratory disorders and dyslipidemia. Obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure. Novel lipid dependent, metabolic risk factors associated to obesity are the presence of the small dense LDL phenotype, postprandial hyperlipidemia with accumulation of atherogenic remnants and hepatic overproduction of apoB containing lipoproteins. All these lipid abnormalities are typical features of the metabolic syndrome and may be associated to a pro-inflammatory gradient which in part may originate in the adipose tissue itself and directly affect the endothelium. An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. The current review will focus on these aspects of lipid metabolism in obesity and potential interventions to treat the obesity related dyslipidemia.
1,086 citations
TL;DR: Treatment with an insulin-sensitizing agent, such as metformin, in patients with type 2 diabetes mellitus may correct several of the primary pathophysiological abnormalities of the metabolic syndrome.
Abstract: Metformin is an insulin-sensitizing agent with potent antihyperglycemic properties. Its efficacy in reducing hyperglycemia in type 2 diabetes mellitus is similar to that of sulfonylureas, thiazolidinediones, and insulin. Metformin-based combination therapy is often superior to therapy with a single hypoglycemic agent. The antihyperglycemic properties of metformin are mainly attributed to suppressed hepatic glucose production, especially hepatic gluconeogenesis, and increased peripheral tissue insulin sensitivity. Although the precise mechanism of hypoglycemic action of metformin remains unclear, it probably interrupts mitochondrial oxidative processes in the liver and corrects abnormalities of intracellular calcium metabolism in insulin-sensitive tissues (liver, skeletal muscle, and adipocytes) and cardiovascular tissue.
1,086 citations
TL;DR: In multivariate analysis, low Kg and high serum insulin levels independently increased the risk for developing diabetes among the offspring of diabetic parents, suggesting that the primary defect is in peripheral tissue response to insulin and glucose, not in the pancreatic beta cell.
Abstract: Objective: To determine whether insulin resistance or insulin deficiency is primary in the pathogenesis of type II diabetes. Design: Cohort analytic study of persons with normal glucose tolerance b...
1,086 citations
TL;DR: Additional evidence is presented by showing that in baboons the infusion of exogenous insulin into the CSF elicits a reliable and predictable decrease in food intake and body weight.
Abstract: Body adiposity is normally maintained within rigid limits1–3. Although it is not clear that this regulation fits a strict negative feedback pattern, animals do maintain a relatively constant body adiposity4. It has been postulated that this regulation is mediated by some signal which informs centres controlling food intake, probably located in the brain, as to the present state of adiposity5,6. The identity of the signal is unknown, but the direct correlation between body adiposity and basal insulin levels in the plasma7–9, suggests insulin as a possible candidate. This hormone is present in the cerebrospinal fluid (CSF) of many species10–13, and is a slow integral over time of the level within the plasma14. Thus, the level of insulin in the CSF is relatively resistant to short-term plasma fluctuations of insulin. Obese humans have higher levels of CSF insulin than lean controls and the CSF insulin level of both obese and lean humans is reduced proportionately after a prolonged fast15. We have therefore postulated16 that the feedback system responding to body adiposity uses the concentration of insulin in the CSF as a major signal. Additional support for such a role is found in recent reports that insulin receptors are present in several regions of the brain and spinal cord17–20. We now present additional evidence for our hypothesis by showing that in baboons the infusion of exogenous insulin into the CSF elicits a reliable and predictable decrease in food intake and body weight.
1,083 citations