Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of hypertension among the obese is twice as high as that in persons of normal weight. Not only the BMI, but, and in particular, the circumference of the waist correlates with blood pressure. A relationship also obtains between BMI and left-ventricular muscle mass, with left-ventricular hypertrophy occurring twelve times more often among the obese than among slim persons. Obesity puts a strain on both the hemodynamics and metabolism of the heart. On the one hand, long-term sequelae include disordered cardiac function extending to cardiomyopathy, on the other, obesity is responsible for sympatho-adrenergic stimulation considered to be a cause of insulin resistance, and is thus, in particular in the hypertensive, closely associated with metabolic syndrome. Specific nondrug treatment options include weight reduction, a low-salt diet and physical exercise. In some cases, Sibutramine and Orlistat may have a supporting role. For the antihypertensive treatment of the obese, drugs with a favorable hemodynamic and metabolic effect should be used.
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PMID:[Hypertension and cardiomyopathy in obesity. Treat the heart simultaneously]. 1169 85

We evaluated the glucose and lipid metabolism in 65 patients (aged 1.1-55 years) with mulibrey (muscle-liver-brain-eye) nanism (MUL), which is a monogenic disorder with prenatal-onset growth failure and typical clinical characteristics. MUL is caused by mutations in the TRIM37 gene, encoding a peroxisomal protein (TRIM37) with E3 ubiquitin-ligase activity. The subjects underwent clinical evaluation, abdominal ultrasonography, and laboratory measurements, including a 3-h oral glucose tolerance test. The results showed a dramatic change in glucose and lipid metabolism with age in MUL subjects. While the children had low fasting glucose and insulin levels, 90% of the adults had high fasting and postload insulin values (up to 1,450 mU/l). A 10-fold decrease in the fasting glucose-to-insulin ratio and a 4-fold decrease in whole-body insulin sensitivity index were observed. Insulin resistance, fatty liver, high serum leptin, hypertension, and acantosis nigricans were already evident in many slim prepubertal children. Half of the adults had type 2 diabetes, and an additional 42% showed impaired glucose tolerance. Seventy percent fulfilled the National Cholesterol Education Program criteria for metabolic syndrome. The peroxisomal targeting and the functional link of TRIM37 to the ubiquitin-proteosome pathway may provide novel clues to the development of metabolic syndrome.
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PMID:Insulin resistance syndrome in subjects with mutated RING finger protein TRIM37. 1630 79

Differentiation of the various forms of diabetes is necessary for therapeutic reasons. Typical signs of type 2 diabetes are age over 40, obesity, and other markers for metabolic syndrome, a positive famitory, gradual development of the classical symptoms, and no evidence of ketosis. It is important to distinguish this from LADA (latent autoimmune diabetes of adulthood), a form of type 1 diabetes mellitus. To establish this differential diagnosis antibody testing is employed. Antibody tests in patients with newly manifest diabetes make good sense when the clinical diagnosis is not unequivocal, that is, to distinguish it from type 2 diabetes, MODY diabetes, hereditary and secondary forms. At present, immunodiagnosis is used too often in unambiguous cases of type 1 diabetes, but too rarely in supposed type 2 diabetes. As a rule, LADA patients are GADA-positive. If MODY diabetes is suspected, a genetic examination is indicated. In patients with GDM, antibody testing with GADA makes sense, in particular in slim patients receiving insulin treatment, since these patients have a high risk for developing a postpartum diabetes already in the first years.
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PMID:[Diabetes mellitus--differential diagnosis]. 1680 91

Clinical similarities between Cushing's syndrome and obesity/metabolic syndrome have led to speculation of a role for glucocorticoids (GCs) in the etiopathogenesis of obesity. People with idiopathic obesity have normal circulating cortisol concentrations. However, there may be considerable interindividual variation in GC sensitivity. The objective of this study was to determine whether enhanced GC sensitivity in the absence of GC excess was a characteristic of obese people with cushingoid features. We studied 12 obese subjects with cushingoid features in the absence of Cushing's syndrome and six slim control participants. Data recorded included BMI, waist-to-hip ratio, blood pressure, glucose and insulin response to 75 g oral glucose challenge, and low-dose (0.25 mg) overnight dexamethasone (DEX) suppression test (ODST-0.25 mg). To study GC-sensitivity in vitro, we performed dose-response studies of DEX-induced suppression of interleukin-6 (IL-6) secretion in skin fibroblast cultures. Seven obese subjects were normosensitive and five subjects hypersensitive to GCs in vitro. ODST-0.25 mg resulted in a median suppression of cortisol from baseline of 32% in normosensitive and 60% in hypersensitive obese subjects (P < 0.004). No other clinical or biochemical measures were discriminatory between these two groups. These data from two independent measures of GC sensitivity suggest that enhanced GC sensitivity may characterize a substantial proportion of obese people with cushingoid appearance.
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PMID:In vivo and in vitro glucocorticoid sensitivity in obese people with cushingoid appearance. 1871 48

Klinefelter's syndrome (KS) is the most common sex-chromosome disorder in men, affecting approximately 1:660 men, and is a rather common cause of infertility, hypogonadism and learning disability. Traditionally, men with KS have been described as tall, slim, narrow shouldered, broad hipped, with hypergonadotrophic hypogonadism and small testes. Recent studies showed an increased risk of diabetes and an unfavourable change in body composition; with accumulation of body fat and decreased muscle mass and a concomitant decrease in insulin sensitivity, muscle strength and oxygen consumption capacity. Here, we review the data on body composition, insulin resistance and metabolic syndrome in relation to testosterone in both KS patients and normal men. Treatment with testosterone in hypogonadal states (other than KS) seems to improve body composition in both clinical and experimental studies. Despite the lack of such studies in KS, we recommend testosterone treatment to KS patients with low serum testosterone or increased LH and change in body composition.
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PMID:Klinefelter's syndrome, type 2 diabetes and the metabolic syndrome: the impact of body composition. 2023 Nov 62

In Japan, the number of low weight birth babies is increasing. The increase in the number of slim young women is considered to be associated with the rising number of low birth weight babies in Japan. In 1993, Barker et al. published highly influential findings indicating a relationship between low birth weight and increased risk of developing symptoms of metabolic syndrome. Here, we report on results that occur when dietary restriction is applied during all periods of pregnancy. It was shown that, at 5 d, the mean weight of pups in the dietary restriction group was lower than the mean weight of pups in the control group. Catch-up growth began when milk yields of the dietary restriction group pups attained the same levels as those of the control group pups. Intra-abdominal adipose tissue weights of the dietary restricted group were significantly higher than those of the control group in males at 280 d after birth. Intra-abdominal adipose tissue weights of the dietary restricted group had a tendency to be higher than those of the control group for female rats. In male rats, it is considered that increase in intra-abdominal adipose tissue is related to lean body mass but it is not related to the function of brown adipose tissue (BAT). In female rats, it is considered that the increase in intra-abdominal adipose tissue is related to the function of BAT and lean body mass.
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PMID:Effect of severe maternal dietary restriction on growth and intra-abdominal adipose tissue weights in offspring rats. 2122 99

Every year, scores of millions of people - as diverse as obese and lean, teenagers and older adults, sedentary and elite athletes, commoners and celebrities - attempt to lose weight on some form of diet. They are often encouraged by their parents, friends, health professionals, training coaches, a media that promotes a slim image and a diet-industry that in Europe and United States alone has an annual turnover in excess of $150 billion. Weight regain is generally the rule, with one-third to two-thirds of the weight lost being regained within 1 year and almost all is regained within 5 years. With studies of the long-term outcomes showing that at least one-third of dieters regain more weight than they lost, together with prospective studies indicating that dieting during childhood and adolescence predicts future weight gain and obesity, there is concern as to whether dieting may paradoxically be promoting exactly the opposite of what it is intended to achieve. Does dieting really make people fatter? How? Does dieting increase the risks for cardiometabolic diseases as many go through repeated cycles of intentional weight loss and unintentional weight regain, i.e. through yo-yo dieting or weight cycling? What's new in adipose tissue biology pertaining to the mechanisms that drive weight regain? Why does exercise not necessarily work in concert with dieting to achieve weight loss and prevent weight regain? What 'lessons' are we learning from bariatric surgery about the mechanisms by which long-term weight loss seems achievable? It is these questions, against a background of preoccupation with dieting, that recent advances and controversies relevant to the theme of 'Pathways from dieting to weight regain, to obesity and to the metabolic syndrome' are addressed in this overview and the eight review articles in this supplement reporting the proceedings of the 7th Fribourg Obesity Research Conference.
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PMID:Pathways from dieting to weight regain, to obesity and to the metabolic syndrome: an overview. 2561 98