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The human disease lipoatrophic (or lipodystrophic) diabetes is a rare syndrome in which a deficiency of adipose tissue is associated with Type 2 diabetes. This disease is an interesting contrast to the usual situation in which diabetes is associated with obesity, an excess of fat. Aside from obesity, patients with lipodystrophic diabetes have the other features associated with Metabolic Syndrome X, including hypertension and dyslipidemia. The contrast between diabetes with a lack of fat and diabetes with an excess of fat provides an opportunity to study the mechanisms causing Type 2 diabetes and its complications. Recently, three laboratories have produced transgenic mice that are deficient in white adipose tissue. These mice have insulin resistance and other features of lipoatrophic diabetes, and are a faithful model for the human disease. Here we review the different murine models of fat ablation and compare the murine and human diseases, addressing the questions: Is the lack of fat causative of the diabetes, and if so by what mechanism? How could the other clinical features be explained mechanistically? And finally, what can be gleaned about insight into treatment options?
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PMID:Transgenic mice lacking white fat: models for understanding human lipoatrophic diabetes. 1084 69

Metabolic syndrome X is a multifaceted syndrome, which occurs frequently in the general population. It is more common in men than in women. A large segment of the adult population of industrialized countries develops the metabolic syndrome, produced by genetic, hormonal and lifestyle factors such as obesity, physical inactivity and certain nutrient excesses. This disease is characterized by the clustering of insulin resistance and hyperinsulinemia, and is often associated with dyslipidemia (atherogenic plasma lipid profile), essential hypertension, abdominal (visceral) obesity, glucose intolerance or noninsulin-dependent diabetes mellitus and an increased risk of cardiovascular events. Abnormalities of blood coagulation (higher plasminogen activator inhibitor type 1 and fibrinogen levels), hyperuricemia and microalbuminuria have also been found in metabolic syndrome X. This review summarizes the present knowledge of abnormalities in this syndrome. Each risk factor is reviewed, and potential criteria for diagnosis and therapeutic targets are discussed. Because patients with metabolic syndrome X accumulate cardiac risk factors, they should be given special attention in terms of diagnosis and treatment.
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PMID:Metabolic syndrome X: a review. 1086 69

The introduction of HAART has changed the nutritional status of HIV patients. In the pre-protease inhibitor (PI) era, more than 60% of HIV-positive persons presented with protein energy malnutrition (PEM) and vitamin and mineral deficit. This caused progressive physical-metabolic wasting (wasting syndrome/cachexia) and increased susceptibility to opportunistic infections and drug toxicity. PEM was a concurrent cause in 80% of deaths attributed to AIDS. Since 1996, the year in which PIs were introduced, the number of patients dying as a result of AIDS has decreased by two thirds, and cachexia is no longer the AIDS terminal phase in developed countries. But different patterns of nutritional status changes have appeared in association with the use of newer anti-HIV therapies and with longer survival of HIV-infected patients. A new clinical and laboratory syndrome--lipodystrophy syndrome--now affects patients receiving PI-based therapy. This syndrome consists of changes in body shape that are caused by an abnormal redistribution of fat. Fat accumulates in the abdominal area (truncal and visceral obesity), in the axillary pads (bilateral symmetric lipomatosis), and in the dorsocervical pads ("buffalo hump," "bull neck") but decreases in the legs, arms, and nasolabial and cheek pads (peripheral lipodystrophy). Hyperlipidemia and insulin resistance are also frequently present (metabolic syndrome X). Pathogenic mechanisms of lipid and fat tissue disturbances are discussed in this article, and the clinical approach to patient management and therapeutic options for lipodystrophy and lipid dysmetabolism is evaluated.
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PMID:Reversal of cachexia in patients treated with potent antiretroviral therapy. 1088 68

The author submits a review on the combined prevalence of diabetes and hypertension which increases with age and is a basic risk factor of vascular cardiac and cerebral complications. It is associated with a higher incidence of obesity, hypertriglyceridaemia and reduced HDL-cholesterol. It is part of the metabolic syndrome X, the syndrome of insulin resistance. Hypertension is found in 60-80% type 2 diabetics and in 40% type 1 diabetics. Obesity is found on average in 40% type 1 diabetics and 85% type 2 diabetics. Macroangiopathy leads to ischaemic heart disease, cerebrovascular episodes and ischaemia of the lower extremities. British investigations revealed that long-term intensive control of the blood sugar level and hypertension reduced in particular the incidence of microvascular complications. A marked decline of the morbidity and mortality of diabetics was recorded after effective treatment of hypertension maintaining blood pressure readings below 130/80 mm Hg. The author discusses also contemporary views on the etiopathogenesis of hypertension in diabetic subjects who may suffer from different types of hypertension. The combination of diabetes and hypertension has obviously a multifactorial etiology--genetic predisposition and several external mechanisms. In the pathogenesis of hypertension an important part is played by insulin resistance and enhanced activity of the sympathetic nervous system. Reaven's hypothesis of metabolic syndrome X was supplemented in recent years by the role of the sympathoadrenal system. From the therapeutic aspect effective reduction of hypertension by correct selection of antihypertensives is most important.
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PMID:[Hypertension and diabetes mellitus--pathophysiology and risk]. 1095 57

Multiple metabolic syndrome (MMS) implies a frequent coincidence of four basic serious metabolic risk factors for subsequent manifestation of cardiovascular disease. The latter include: central type obesity, arterial hypertension, dyslipoproteinaemia and diabetes mellitus type II (non-insulin-dependent diabetes mellitus--NIDDM). MMS is also described as syndrome X, Reaven's syndrome, insulin resistance syndrome, metabolic syndrome or as the "deadly quartet". NIDDM in humans is conceived as a syndrome the pathogenesis of which is multifactorial and it is not an unequivocal nosological unit. It many epidemiological studies reliable evidence was provided that in the aetiology of NIDDM a marked genetic influence is involved. Its genetic predisposition is conditioned by the interaction of candidate genes and a complex of influences of the external environment. Evidence was provided that MMS phenotypes cumulate only in members of some families. The mode of genetic transmission of NIDDM remains obscure.
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PMID:[Genetic predisposition for multiple metabolic syndrome. Part 1. Diabetes mellitus type 2--incidence and prevalence]. 1095 28

Risk factors contributing to the potential inter-relationship between obesity and hypertension include insulin, fatty acids, and angiotensin II. All of these mediators are either produced by or act on adipocytes, influence fat cell metabolism, and have effects on the cardiovascular system. Moreover, these three mediators have several potential sites for positive feedback interaction, thus exacerbating the influence of any single risk factor. The purpose of this review is to highlight recent advances in our understanding of the influence of insulin, fatty acids, and angiotensin II on fat cell metabolism. Special emphasis is placed on potential adipose-related mechanisms of these factors, which would predictably elevate blood pressure. Given the prevalence of obesity and hypertension in the American population, delineation of potential pharmacologic targets that would influence both of these disease states is of primary importance to the successful treatment of these diseases of the metabolic syndrome X.
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PMID:Fat cell metabolism: insulin, fatty acids, and renin. 1098 Nov 39

Metabolic syndrome X includes glucose intolerance or type 2 diabetes, dyslipidemia and arterial hypertension which are classical cardiovascular (CV) risk factors. In course of time, other CV risk factors have been added to the syndrome: rheological alterations, endothelial dysfunction, anomalies in the coagulation/fibrinolysis system, microalbuminuria and so on.... Insulin resistance is the cornerstone of metabolic syndrome X, with secondary hyperinsulinism. Upper body obesity is associated with metabolic syndrome X. Simple waist measurements can detect the subjects (10-15% of the population) at increased CV risk with a sensitivity of 70%. This is invaluable for such a simple and cheap test. Diet is the first step in treating these patients and reducing caloric intake is necessary in most of them. Saturated fats will be replaced by polyunsaturated and mono-unsaturated ones. Long-chain carbohydrates with low glycemic index will be suggested. Regular physical activity will be promoted. If these life style modifications fail, drugs can be added: biguanide and glitazone are good candidates. Orlistat has improved metabolic syndrome X on a long-term basis. Drugs that could increase insulin resistance are to be avoided.
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PMID:[The importance of syndrome X in daily practice]. 1119 91

The author exposes the present concept of metabolic syndrome X, which is a complex of Type II diabetes, obesity, hypertension and vascular problems. This syndrome has been known for many years, but it has been individualized as such only recently. This is due to the huge importance that obesity is reaching in developed countries, especially in the U.S.A. Today this is a very important health problem. In this work, in addition to the description of the syndrome, which is purely an internal medicine issue, its relation to some women-specific problems is also explained, especially to the so-called polycystic ovary.
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PMID:[Metabolic syndrome X in women]. 1120 48

The discovery of a link between in utero experience and later metabolic and cardiovascular disease is one of the most important advances in epidemiology research of recent years. There is increasing evidence that alterations in the fetal environment may have long-term consequences on cardiovascular, metabolic, and endocrine pathophysiology in adult life. This process has been termed programming, and we have shown that undernutrition of the mother during gestation leads to programming of hyperphagia, obesity, hypertension, hyperinsulinemia, and hyperleptinemia in the offspring. Using this model of maternal undernutrition throughout pregnancy combined with postnatal hypercaloric nutrition of the offspring, we examined the effects of IGF-I therapy. Virgin Wistar rats (age 75 +/- 5 d, n = 20 per group) were time mated and randomly assigned to receive food either ad libitum or 30% of ad libitum intake (UN) throughout pregnancy. At weaning, female offspring were assigned to one of two diets (control or hypercaloric [30% fat]). Systolic blood pressure was measured at day 175 and following infusion with 3 microg/g per day recombinant human IGF-1 (rh-IGF-I) by minipump for 14 d. Before treatment, UN offspring were hyperinsulinemic, hyperleptinemic, hyperphagic, obese, and hypertensive on both diets, compared with ad libitum offspring and this was exacerbated by hypercaloric nutrition. IGF-I treatment increased body weight in all treated animals. However, systolic blood pressure, food intake, retroperitoneal and gonadal fat pad weights, and plasma leptin and insulin concentrations were markedly reduced with IGF-I treatment. IGF-I treatment resulted in a 3- to 5-fold increase in 38--44 kDa and 28--30 kDa IGF binding proteins, although in UN animals, there was an impaired and differential up-regulation of these insulin-like growth factor binding proteins following IGF-I treatment. The 24-kDa IGF binding protein representing IGF binding protein-4 was down-regulated in all IGF-I-treated animals, but the decrease was more marked in UN animals. Our data suggest that IGF-I treatment alleviates hyperphagia, obesity, hyperinsulinemia, hyperleptinemia, and hypertension in rats programmed to develop the metabolic syndrome X.
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PMID:IGF-I treatment reduces hyperphagia, obesity, and hypertension in metabolic disorders induced by fetal programming. 1151 75

The underlying determinants of cardiovascular risk are governed by both genetic and lifestyle factors. One of the major adverse outcomes of unhealthy lifestyles is obesity, the genesis of which begins in childhood. Obesity, an important risk factor for atherosclerotic cardiovascular disease, type 2 diabetes, and hypertension, persists (tracks) strongly from adolescent years to adulthood. Secular trends toward increased obesity in the past 25 years have occurred in children and adults alike. Of interest, baseline adiposity precedes hyperinsulinemia in all age groups, independently of race, sex, and baseline insulin levels. Adiposity is an independent predictor of the risk of developing the cluster of risk variables of the metabolic syndrome X, beginning in childhood. Exposure to a multiple risk factor burden over time enhances the development of coronary atherosclerosis and hypertensive cardiovascular disease. In fact, autopsy studies in youths have shown that the extent of fibrotic atherosclerotic plaques in coronary arteries, measured antemortem, increases markedly with the presence of syndrome X risk variables. Further, in overweight children, insulin levels are associated with left ventricular mass. In young people, overnutrition, coupled with physical inactivity, leads to weight gain. Since obesity, unhealthy dietary habits, and a sedentary lifestyle are interrelated and modifiable, prevention and intervention must begin in early life. (c)2001 CHF, Inc.
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PMID:Emergence of obesity and cardiovascular risk for coronary artery disease: the Bogalusa Heart Study. 1182 87


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