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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The medical effects of modest weight reduction (approximately 10% or less) in patients with obesity-associated medical complications were reviewed. The National Library of Medicine MEDLINE database and the Derwent RINGDOC database were searched to identify English language studies that examined the effects of weight loss in obese patients with serious medical complications commonly associated with obesity (non-insulin dependent diabetes mellitus (NIDDM or type II), hypertension, hyperlipidemia, hypercholesterolemia, and cardiovascular disease). Studies in which patients experienced approximately 10% or less weight reduction were selected for review. Studies indicated that, for obese patients with NIDDM, hypertension or hyperlipidemia, modest weight reduction appeared to improve glycemic control, reduce blood pressure, and reduce cholesterol levels, respectively. Modest weight reduction also appeared to increase longevity in obese individuals. In conclusion, a large proportion of obese individuals with NIDDM, hypertension, and hyperlipidemia experienced positive health benefits with modest weight loss. For patients who are unable to attain and maintain substantial weight reduction, modest weight loss should be recommended; even a small amount of weight loss appears to benefit a substantial subset of obese patients.
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PMID:Beneficial health effects of modest weight loss. 132 66

Previous studies have shown that patients with non-insulin dependent diabetes mellitus (NIDDM) have a higher metabolic rate (RMR) and lower thermogenesis in comparison with persons with normal glucose tolerance. It is not clear whether this impairment is due to the diabetic state per se or to the association of the diabetic and obese state. The impact of obesity on RMR and glucose-induced thermogenesis (GIT) was studied in seven non-obese and 12 obese men with NIDDM; the results are compared with a group of six obese men with normal glucose tolerance. RMR was significantly higher for the obese subjects (P < 0.02) but this difference disappeared after correction for fat-free mass. Mean GIT was significantly lower (P < 0.01) in the diabetic patients, whether they were obese or non-obese. The results of this study indicate that for patients with NIDDM, the impact of obesity on both RMR and GIT is rather limited. On the other hand, a significant influence of glucose tolerance on GIT in obese patients could be demonstrated.
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PMID:Impact of obesity on resting metabolic rate and glucose-induced thermogenesis in non-insulin dependent diabetes mellitus. 133 Sep 61

The obvious syntropy of obesity and type II (non-insulin dependent) diabetes mellitus has always suggested a causal inter-relationship between the two diseases. However, the actual pathophysiological connection still remains to be elucidated. Recent findings have suggested that insulin resistance and hyperinsulinaemia might link glucose intolerance/type II diabetes mellitus, hypertension and hyperlipoproteinaemia in the context of a hypothetical 'syndrome X' characterized by an excessive risk constellation for the development of atherosclerosis. However, as to the practical consequences of the ('diabesity') syndrome of type II diabetes mellitus and structured programmes for effective therapy, very little new information has been gathered during the past 100 years.
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PMID:Risk of obesity in type II diabetes mellitus. 133 84

Lipoprotein(a) [Lp(a)] has been added to the list of independent risk factors for cardiovascular disease (CVD), whose incidence is greater in obese subjects. There are few data available on the serum Lp(a) concentrations in obese individuals with or without insulin dependent diabetes mellitus (NIDDM). We selected 31 obese men with normal glucose tolerance (NGT) tests, 15 obese diabetic men, 14 non obese diabetic men and 17 healthy men as controls. We measured serum total cholesterol, HDL cholesterol, triglycerides, glucose, insulin and Lp(a). The mean Lp(a) levels in NGT obese men were 70.00 +/- 13.40 mg/l, which were similar to those found in normal controls (75.98 +/- 24.70 mg/l); significantly higher mean Lp(a) levels were found in obese diabetic men (168.84 +/- 56.43 mg/l) and in non obese diabetic men (240.85 +/- 63.35 mg/l). No significant correlation between Lp(a) levels and age, body mass index (BMI), total cholesterol, HDL cholesterol, triglycerides, insulin, was found; only a significant positive correlation between Lp(a) levels and glucose could be revealed (P < 0.05). Since higher levels of Lp(a) were found in NIDDM subjects with or without obesity, we conclude that hyperglycemia may influence the levels of serum Lp(a) facilitating its glycosylation in the liver with the consequence of a decline in its catabolic rate.
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PMID:Serum lipoprotein Lp(a) in obesity. 134 6

1. To determine the effects of gene dilution on development of IGT, NIDDM and in vitro glucose oxidation, heterozygous lean LA/N-cp female and SHR/N-cp male rats were mated, and F1 offspring studied at periodic intervals to determine the prevalence of obese and diabetic traits. 2. Obesity occurred in 25% of offspring by 5 weeks of age, consistent with inheritance of the autosomal recessive cp trait. 3. IGT occurred in all obese male F1, 67% of obese female F1, and 18% of the lean male F1 rats by 5 months of age, and diabetes occurred in 80% of male obese and 17% of female obese rats from 6 months of age. Glycosuria occurred with glucose intolerance, and was more severe in rats with NIDDM than IGT. 4. Rates of in vitro glucose oxidation were greater in diaphragm and adipose tissue, and were greater in the presence of insulin (100 mu Units/ml) in obese female but not obese male F1 rats. 5. These results indicate that the development of glucose intolerance is more prominent in male than in female F1 rats, that the progression of IGT to NIDDM occurs later in life in the F1 hybrid than in the SHR/N-cp strain from which the diabetic trait was transmitted, and that genetic dilution of the diabetic trait via hybrid breeding results in a delay in the expression of NIDDM which is chronologically more similar to that which occurs in man.
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PMID:Effect of genetic dilution on development of diabetes, impaired glucose tolerance and in vitro glucose oxidation in LA/N-cp x SHR/N-cp F1 hybrid rats. 134 69

Obesity is a multifactorial disease with a marked genetic component. The situation is further complicated by the heterogeneity of obesity demonstrated by the topographical distribution of body fat, e.g. upper body (central) and lower body (gluteal) obesity. Furthermore, the distribution of fat shows a stronger heritable tendency compared with total body fat. Central obesity is characterized by hyperinsulinaemia and insulin resistance, a feature in common with non-insulin dependent diabetes mellitus, hypertension and atherosclerosis. In order to study the molecular genetics of central obesity we have examined 56 severely obese (mean body mass index 40), unrelated British Caucasoid young non-diabetic women for associations of restriction fragment length polymorphism of candidate genes with anthropometric measurements and indices of insulin secretion and resistance. The candidate genes examined were insulin receptor, insulin sensitive glucose transporter and insulin. An association of the class 3 allele of the hypervariable region in the 5' flanking region of the insulin gene was found with upper segment obesity (P = 0.005). Furthermore, the class 3 allele was also associated with fasting hyperinsulinaemia (P = 0.01), stimulated insulin secretion (P = 0.01) and insulin resistance as calculated from the homeostatic model of assessment (HOMA; P = 0.008). No such associations were found with the other candidate genes studied. This data suggests that polymorphisms in the 5' flanking region of the insulin gene may affect expression of the gene and thereby modulate insulin production in severely obese female subjects.
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PMID:Central obesity and hyperinsulinaemia in women are associated with polymorphism in the 5' flanking region of the human insulin gene. 135 60

Non-insulin-dependent diabetes mellitus (NIDDM) is an important health problem in the black population of southern Africa. Whether the primary cause of NIDDM is insulin secretory dysfunction or peripheral insulin resistance is unknown. In westernised populations it is believed that insulin resistance and hyperinsulinaemia occur in the early stages of disease, followed later by progressive impairment of insulin secretion. However, we suggest that in the southern African black population a decrease in the mass of functioning beta cells is an important event, making these people vulnerable to the deleterious effects of insulin resistance induced by obesity and other factors. These abnormalities are, in turn, associated with insulin receptor down-regulation. An accelerated decline in beta-cell function then follows in susceptible individuals, ultimately producing striking insulinopenia. Insulinopenic NIDDM in black southern Africans may partly explain why this population has a comparatively low incidence of macrovascular complications and also predicts a short-lived therapeutic response to oral sulphonylureas in most patients.
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PMID:Pathogenesis of non-insulin-dependent diabetes mellitus in the black population of southern Africa. 135 91

In recent decades, non-insulin dependent diabetes mellitus (NIDDM) has become a major public health problem in several parts of the world. A complex disorder, NIDDM is associated with an increased risk of blindness, coronary heart disease, peripheral vascular disease, and kidney failure (1). The epidemiology of NIDDM is providing new insights into many aspects of this disease, including prevalence, incidence, morbidity, and mortality (2). My objective is to explain the high prevalence of a NIDDM susceptible genotype(s) in several distinct populations: American Indians, Australian Aborigines, and Pacific Islanders. The susceptible genotype may have been selected into these populations because of unusually frequent food shortages that occurred during the initial colonization of 'new worlds'. NIDDM has been shown to have a strong genetic component (3) that may include a 'thrifty' genotype(s) (4,5). The 'thrifty' genotype(s) may have once allowed founding populations to survive feast' and 'famine' conditions for several generations. With an assured food supply and a sedentary lifestyle, however, the 'thrifty' genotype(s) becomes disadvantageous, leading to obesity, increased insulin resistance, beta cell decompensation, and NIDDM (3,6).
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PMID:Archaeology and the "thrifty" non insulin dependent diabetes mellitus (NIDDM) genotype. 136 87

The significance of variation within the genes coding for three glucose transporter proteins in the aetiology of non-insulin dependent diabetes mellitus was assessed by analysing restriction fragment length polymorphisms in an English Caucasian population. Two polymorphisms at the HepG2/erythrocyte glucose transporter (GLUT1) locus, four at the liver/pancreatic glucose transporter (GLUT2) locus and one at the muscle/adipocyte glucose transporter (GLUT4) were analysed in a sample of diabetic and non-diabetic subjects. No significant differences in the allelic, genotypic or haplotypic frequencies of the polymorphisms at these three loci were observed between the diabetic or non-diabetic populations. No significant linkage disequilibrium was observed between the two GLUT1 polymorphic sites, whereas the four polymorphic sites at the GLUT2 locus, one of which appears to be due to a 100-200 base pair DNA insertion/deletion, were found to be in significant linkage disequilibrium. In order to study the possible role of glucose transporter gene variants contributing to the development of obesity, the body mass indexes were compared in the different genotypic groups of diabetic and non-diabetic subjects. No differences in body mass index between genotype groups were found at the p < 0.005 level of significance.
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PMID:Analysis of three glucose transporter genes in a Caucasian population: no associations with non-insulin-dependent diabetes and obesity. 136 30

The efficiency of clearance of plasma triacylglycerols (TAG) after fatty meals in non-diabetic Caucasian subjects is believed to determine the plasma level of high-density-lipoproteins-cholesterol (HDL-C). It is unknown if this observation holds in diabetic subjects and in other racial groups. In assessing the factors that determine TAG responses to acute fat loading in a tropical African population with a low prevalence of atherosclerotic disease, twenty (nine obese) non-insulin-dependent diabetic (NIDDM) patients with optimal glycaemic control and twelve (six obese) age-matched non-diabetic subjects were given meals containing 50 g fat (in butter) and 75 g carbohydrate (in white bread) over 15 min in the morning after a 12 h overnight fast. The fasting plasma levels of glucose, TAG, total cholesterol (total-C), HDL-C, low-density-lipoprotein-cholesterol, insulin and glycosylated haemoglobin (HBAlc) were estimated; glucose and TAG levels were also measured postprandially for 8 h at 2 h intervals. Postprandial lipaemia was consistently higher in the diabetic patients (about 50-100% more than values obtained in the non-diabetic subjects, even when corrected for differences in body mass) and correlated positively with age and postprandial glycaemia. This defect in TAG clearance was even worse (by about 50%) when glucose tolerance became further impaired after ten of the diabetic patients stopped oral hypoglycaemic treatment for 1 week and the fat-tolerance test was repeated. In the obese non-diabetic subjects, but not those of normal weight, there were significant negative relationships between the postprandial lipaemia and fasting plasma levels of HDL-C and HDL-C: total-C ratio, as reported in Caucasians. It is concluded that age and the ambient glucose concentration appear to be the important determinants of the efficiency of TAG clearance in diabetic subjects. This accords with clinical observations of increased atherogenic liability with increasing age and poorer glycaemic control. The determinants in non-diabetic subjects were less defined, indicating that postprandial lipaemia might be influenced by various factors (obesity as shown here) in different subsets of individuals.
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PMID:Some determinants of postprandial lipaemia in Nigerian diabetic and non-diabetic subjects. 139 Jun


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