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

An unfavourable body fat distribution has been associated with an increased prevalence and incidence of non-insulin dependent diabetes mellitus (NIDDM). The potential utility of assessing body fat distribution in diabetes screening, however, has not been assessed. We compared the impact of upper body fat distribution (assessed by the waist-to-hip ratio (WHR)) and body mass index (BMI) and NIDDM using the population attributable risk approach of Levin in 1965 Mexican Americans from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The population attributable risk percentage (PAR%) was 52.0% for WHR compared to 43.4% for body mass index. After stratification by BMI, women with a high WHR had a PAR% of approximately 50% and men had a PAR% of 28-58%. For any given cutpoint (e.g. the 10th percentile, 20th percentile, etc.) of WHR used to screen for NIDDM, WHR had both a higher sensitivity and a lower false positive rate than the corresponding cutpoint of BMI. To evaluate the relative contribution of WHR in identifying prevalent cases of NIDDM, multiple logistic regression analyses were performed, and the number of subjects identified as being in the top 20% of the risk score distribution was compared using a model that included WHR and a model that included BMI. In men, BMI did not increase the sensitivity in detecting NIDDM subjects once age was accounted for; WHR increased the sensitivity only slightly. In women, sensitivity was enhanced modestly using both measures, although WHR again was the more sensitive method. These data suggest that WHR is a better single screening measure for NIDDM than BMI.
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PMID:Public health significance of upper body adiposity for non-insulin dependent diabetes mellitus in Mexican Americans. 131 26

Fluoxetine, an inhibitor of serotonin re-uptake, has been shown to cause weight loss in humans and animals. In order to determine the effects in diabetic subjects, 48 male and female, obese, type 2 non-insulin dependent diabetics being treated with insulin were randomized to receive fluoxetine 60 mg or placebo once daily in double blind fashion for 24 weeks. In all subjects, this treatment was preceded by four weeks and followed by six weeks of single blind placebo washout treatment. Subjects performed daily home glucose monitoring and were given instruction in a 1200 kcal American Diabetes Association diet. Fluoxetine treated subjects who completed the trial (n = 16) lost more weight than placebo treated subjects (n = 20) (9.3 +/- 2.4 vs. 1.9 +/- 2.9 kg +/- s.e.m, P less than 0.05). Subjects in the fluoxetine group also showed a greater percentage decrease in insulin dose than those in the placebo group (46.9 +/- 7.6% vs. 19.3 +/- 7.6%, P less than 0.01). During active treatment, the change in serum glucose levels did not differ between the two groups, while glycohemoglobin fell more in fluoxetine treated subjects than in placebo treated subjects at two of four follow-up visits. These results suggest that fluoxetine may be of benefit in the treatment of obese patients with type 2 non-insulin dependent diabetes mellitus.
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PMID:Fluoxetine treatment of the obese diabetic. 131 28

It is well-known that diabetic patients develop peripheral and autonomic neuropathy, and recent review has also suggested the occurrence of central pathway abnormality in diabetics. In this article, we conducted the BAEP study on 61 cases of NIDDM and 11 cases of IDDM. Peak latency, interpeak latency (IPL) and peak amplitude of BAEPs were analyzed in each case. For further correlation, the motor and sensory nerve conduction velocities of median nerve, the blood sugar, the serum HbA1c were measured. Two nondiabetic groups, age and sex matched with NIDDM and IDDM groups, were used as control. In NIDDM group, the results showed prolongation of all peak latency and IPL except peak latency of wave II and wave IV in the left side and bilateral IPL III-V. There was no statistically significant amplitude difference between NIDDM and age-matched control group. The result of IDDM group revealed prolongation of all peak latency and IPL, except the right IPL III-V. As for amplitude, waves III and V in the right side and waves I and V in the left side were reduced as compared with the age-matched young control group. There was no statistically significant difference in all peak latencies and IPLs between NIDDM and IDDM groups. In both groups of NIDDM and IDDM, the MNCV and SNCV of median nerve were significantly delayed in conduction. The prolongation of III and V peak latency had a linear correlation with their amplitude reduction. In conclusion, both peripheral and central conduction dysfunction occur in both IDDM and NIDDM patients.
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PMID:[Brainstem auditory evoked potentials in diabetes mellitus]. 131 48

In this article we have focused on the evolving pattern of nutritional management of the person with diabetes. Before the advent of insulin in 1922, it was sufficient to identify a meal plan that would keep people alive until they could be rescued from mortality due to diabetic ketoacidosis (the major killer of the era) by pharmacologic means. Now, the life expectancy of people with diabetes is close to that of the general population and focus has turned to combating the new threats of macrovascular disease and kidney failure. Over recent years the susceptibility of NIDDM patients to macrovascular events has been established and the twofold increase in risk of a heart attack in diabetic men is outshadowed by the four- to fivefold risk in diabetic women and the 13- to 17-fold greater risk in diabetics under the age of 30 years compared with their nondiabetic counterparts. The mechanism behind the susceptibility to macrovascular disease has generated a veritable plethora of investigations focusing on the atherogenic profile of diabetic dyslipidemia. Hyperinsulinemia, insulin resistance, and overtreatment of the diabetic with insulin have been claimed as contributors to the development of premature atherosclerosis. The hallmark of the diabetic dyslipidemia is the tendency to elevated VLDL triglyceride levels and the closely linked reduction in HDL cholesterol. Although there is some controversy on the relationship between triglyceride levels and the incidence of CAD, there is no doubt that HDL is an independent risk factor. It can now be safely said that elevated triglycerides are a risk factor in women and that in men elevated triglycerides constitute a risk factor if accompanied by a reduced HDL level. For these reasons, any approach to nutritional management of the diabetic must attempt not only to normalize glycemia but to make every effort to reduce the atherogenic profile. In the accompanying algorithm (Fig. 4), we consider the risk factors conducive to a reduction in life expectancy and offer a meal plan that is appropriate for the individual with diabetes. For the 80% of NIDDM patients who are obese, a diet with a reduction of 500 to 1000 kcal is in order and this may be achieved by a periodic VLCD. We examined carefully the controversy related to yo-yo dieting and support the notion that its effects in humans are not all that harmful. Ingestion of simple sugars in the high carbohydrate diet has negative effects both on carbohydrate and lipid metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The good, the bad, and the ugly in diabetic diets. 131 32

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

To investigate the role of glucagon in the pathogenesis of diabetes, we observed change of plasma glucagon concentrations during glucose loading in normal subjects and patients with impaired glucose tolerance (IGT) and non-insulin dependent diabetes mellitus (NIDDM) using specific radioimmunoassay. The results showed that the fasting plasma glucagon levels in patients with IGT and NIDDM were similar to those of the normal subjects. The nadir of plasma glucagon level in the normal control occurred at 1-h after glucose loading and the changes of glucagon, glucose and insulin levels synchronized; but peaks of plasma glucose and insulin levels in the IGT and NIDDM patients were delayed at 2-h after glucose loading with the lowest glucagon level at 3-h. It was suggested that there were relative hyperglucagonemia and decrease of sensitivity of islet A cell to glucose in IGT and NIDDM patients. The present study also showed that hyperglucagonemia is related to the reduction of insulin secretion and might play an important role in the development of postprandial hyperglycemia in NIDDM.
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PMID:[Changes in plasma glucagon concentration in patients with diabetes mellitus and its clinical significance]. 132 51

Insulin resistance contributes to the pathogenesis of NIDDM. We have investigated the molecular mechanisms of insulin resistance in patients with genetic syndromes caused by mutations in the insulin-receptor gene. In general, patients with two mutant alleles of the insulin-receptor gene are more severely insulin-resistant than are patients who are heterozygous for a single mutant allele. These mutations can be put into five classes, depending upon the mechanisms by which they impair receptor function. Some mutations lead to a decrease in the number of insulin receptors on the cell surface. For example, some mutations decrease the level of insulin receptor mRNA or impair receptor biosynthesis by introducing a premature chain termination codon (class 1). Class 2 mutations impair the transport of receptors through the endoplasmic reticulum and Golgi apparatus to the plasma membrane. Mutations that accelerate the rate of receptor degradation (class 5) also decrease the number of receptors on the cell surface. Other mutations cause insulin resistance by impairing receptor function--either by decreasing the affinity to bind insulin (class 3) or by impairing receptor tyrosine kinase activity (class 4). The prevalence of mutations in the insulin receptor gene is not known. However, theoretical calculations suggest that approximately 0.1-1% of the general population are heterozygous for a mutation in the insulin-receptor gene; the prevalence is likely to be higher among people with NIDDM. Accordingly, it is likely that mutations in the insulin-receptor gene may be a contributory cause of insulin resistance in a subpopulation with NIDDM.
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PMID:Lilly Lecture: molecular mechanisms of insulin resistance. Lessons from patients with mutations in the insulin-receptor gene. 132 27

To examine the release of insulin in response to oral glucose, intravenous glucagon and intravenous arginine, we measured the levels of plasma glucose, immuno-reactive insulin (IRI) and C-peptide levels on fasting and following an oral glucose loading (OGTT), intravenous glucagon (GON) and arginine (ARG) infusion test in nine newly diagnosed non-insulin dependent diabetics. Their ages ranged from 38 to 65. The fasting plasma glucose and hemoglobin A1c levels were 240 +/- 14 mg/dl (Mean +/- SEM) and 10.7 +/- 0.54%, respectively. Mean values of the peak C-peptide/fasting C-peptide ratio and peak IRI/fasting IRI ratio were significantly increased, as compared with the basal level (P < 0.05), but not significantly different from those of the OGTT, GON and ARG test. In conclusion, the effect of arginine-induced insulin secretion in non-insulin dependent diabetes mellitus is as good as those of glucose or glucagon.
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PMID:Arginine induced insulin release in patients with newly onset non-insulin-dependent diabetes mellitus. 133 Feb 42

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 aim of the present study is to explore whether the renal and cardiovascular response to clonidine in type II diabetic patients is different from that in control subjects, and to clarify the role of central alpha 2-receptor in the regulation of cardiovascular response and sodium handling in type II diabetes mellitus (DM). Thirty-five diabetic inpatients aged 30-71 years (54.1 +/- 9.7) and ten control subjects (N) were enrolled in this study after their fasting plasma glucose had been improved. To evaluate the peripheral sympathetic nerve activity, 24-hour urinary catecholamine was measured, and pulse rate (PR) responses to a 30-second standing test was determined. On another day, blood pressure (BP), PR, plasma norepinephrine (PNE), cyclic AMP (p-cAMP), renin activity (PRA), aldosterone (PAC) and growth hormone (p-GH) were measured at 0, 30, 60, 90, 120, 150, 180 minutes following the oral administration of clonidine (150 micrograms). Type II DM were classified as DM with hyper-response (DM-HR, n = 12) when their PR decreased after clonidine more than that of N, and if not, they were classified as DM with normal response (DM-NR, n = 23). Urinary catecholamine excretions in type II DM were within the normal range. BP, PNE and p-cAMP were markedly decreased with clonidine in similar fashion in DM-NR, DM-HR and N. The percent changes of PNE were correlated positively with the changes of p-cAMP in both N and DM-NR (r = 0.660 and 0.449, respectively), but not in DM-HR. No significant difference in the changes of p-GH (delta p-GH) and integral of GH (the area under the curve) following clonidine administration was observed in the three groups. The decrease in PR was correlated with neither delta p-GH (N: r = 0.082, DM-NR: r = -0.400, DM-HR: r = 0.242) or integral of GH (N: r = 0.191, DM-NR: r = 0.382, DM-HR: r = 0.162). The fractional excretion of sodium (FENa) decreased in N (p < 0.01), increased in DM-NR (p < 0.05) and did not change in DM-HR. The changes of FENa were not correlated with those of PRA and PAC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Altered responses of heart rate, renal sodium handling and plasma growth hormone to clonidine in type II diabetic patients]. 133 89


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