1,721,456 research outputs found
Relationship between impaired glucose tolerance, non-insulin-dependent diabetes mellitus and obesity
No full textPlasma glucose concentration is the best predictor for the development of non-insulin-dependent diabetes mellitus (NIDDM). However, obesity is also a recognized risk factor for development of the disease, and is easier to track over time. Thus obesity could be of considerable clinical importance as a predictor of diabetes. Studies have shown that the degree of overweight, the change in weight and the duration of overweight are all separate predictors of diabetes. The British Regional Heart Study showed that an increasing body mass index (BMI) was associated with increased risk of developing diabetes, even at BMI values not considered obese. A separate study showed that weight gain increased the risk of diabetes independently of BMI, while weight loss decreased the risk. The duration of obesity was also an important factor in developing NIDDM. A long duration increased the risk of diabetes, irrespective of the final BMI value. The effects of obesity on insulin action have also been investigated. Studies have shown that insulin sensitivity is inversely related to insulin secretion, with a disproportionate increase in insulin secretion seen with decreasing sensitivity. A recent European study showed that the prevalence of both insulin hypersecretion and insulin resistance increased with increasing BMI. Thus, in obesity, higher insulin levels are necessary to maintain glucose tolerance, leading to increased stress on the β-cells. In obese individuals, weight loss improved insulin sensitivity in proportion to the degree of weight loss, leading to decreased insulin secretion. Weight loss can therefore, at least in the short term, act to decrease the risk of developing diabetes by reducing insulin resistance, and thus relieving β-cell stress, the factor ultimately responsible for hyperglycaemia in predisposed individuals
Role of anatomical location, cellular phenotype and perfusion of adipose tissue in intermediary metabolism: A narrative review
No full textIt is well-established that adipose tissue accumulation is associated with insulin resistance through multiple mechanisms. One major metabolic link is the classical Randle cycle: enhanced release of free fatty acids (FFA) from hydrolysis of adipose tissue triglycerides impedes insulin-mediated glucose uptake in muscle tissues. Less well studied are the different routes of this communication. First, white adipose tissue depots may be regionally distant from muscle (i.e., gluteal fat and diaphragm muscle) or contiguous to muscle but separated by a fascia (Scarpa’s fascia in the abdomen, fascia lata in the thigh). In this case, released FFA outflow through the venous drainage and merge into arterial plasma to be transported to muscle tissues. Next, cytosolic triglycerides can directly, i.e., within the cell, provide FFA to myocytes (but also pancreatic ß-cells, renal tubular cells, etc.). Finally, adipocyte layers or lumps may be adjacent to, but not anatomically segregated, from muscle, as is typically the case for epicardial fat and cardiomyocytes. As regulation of these three main delivery paths is different, their separate contribution to substrate competition at the whole-body level is uncertain. Another important link between fat and muscle is vascular. In the resting state, blood flow is generally higher in adipose tissue than in muscle. In the insulinized state, fat blood flow is directly related to whole-body insulin resistance whereas muscle blood flow is not; consequently, fractional (i.e., flow-adjusted) glucose uptake is stimulated in muscle but not fat. Thus, reduced blood supply is a major factor for the impairment of in vivo insulin-mediated glucose uptake in both subcutaneous and visceral fat. In contrast, the insulin resistance of glucose uptake in resting skeletal muscle is predominantly a cellular defect
Hypertension in the Metabolic Syndrome
No full textIn the history of the Metabolic Syndrome hypertension has played a major role because it is the element that has transformed the well known metabolic cluster of obesity dyslipidemia and diabetes into a true syndrome (the sum of apparently different symptoms andsigns). Due to its high prevalence in the population, the difference in diagnostic threshold adopted by the different definitions of the Metabolic Syndrome, although minor, has created some confusion with regard to its epidemiology and its ability to predict diseases. The Metabolic Syndrome recognizes environmental, ethnic and genetic influences; however, in this respect hypertension appears different with respect to the metabolic elements of the syndrome that seem to be under a stronger genetic influence. Beyond genetics there are also physiopathologic explanations for the association of hypertension with the Metabolic Syndrome that involve arterial stiffness, the sympathetic nervous system and the hypothalamic, pituitary, adrenal axes. The possibility that arterial hypertension (hemodynamically) might favour the Metabolic Syndrome is extremely unlikely. The influence of hypertension on metabolism may also be mediated through the metabolic effect of antihypertensive drugs. Although no controlled study has addressed this issue yet, we extrapolate the data concerning the effect of antihypertensive drugs on development of diabetes. We conclude that this possibility is unlikely
Association between glycosuria and albuminuria in patients with type 2 diabetes from the CREDENCE trial: a mechanistic link?
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Determinants and pathological role of insulin hypersecretion in nondiabetic adults and adolescents
No full textTHE TOXIC EFFECTS OF CLOFIBRATE AND ITS METABOLITE ON MAMMALIAN SKELETAL MUSCLE: AN ELECTROPHYSIOLOGICAL STUDY
No full textMembrane electrical parameters of rat extensor digitorum longus muscles were analysed in vitro, with intracellular microelectrodes, after chronic treatment with clofibrate or after in vitro application of chlorophenoxyisobutyric acid, the in vivo metabolite of clofibrate. Clofibrate caused only a 38% decrease in the membrane chloride conductance while its metabolite induced a large decrease of chloride conductance and drastic changes in the excitability characteristics of the muscles sampled. The capability of clofibrate to induce two types of myotonia is discusse
Impaired coronary vasodilator capacity and exercise-induced myocardial ischemia in hypertensive patients are related to pulse pressure
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