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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inheritance of the tendency to develop diet-induced non-insulin-dependent (type II) diabetes was analyzed in crosses between diabetes-prone C57BL/6J (BL/6) mice and diabetes-resistant A/J mice. The effects of a diabetogenic diet on blood glucose and insulin levels, insulin sensitivity, and weight were evaluated in F1 and both (BL/6 X A/J) F1 X BL/6 and (BL/6 X A/J) F1 X A/J backcross mice. These results suggest that diet-induced hyperglycemia is largely determined by a recessive gene and diet-induced insulin resistance by a dominant gene. Analyses of both backcrosses indicated that insulin sensitivity and blood glucose levels were unrelated, suggesting that they are controlled by different genetic factors. This conclusion was supported by data from nine recombinant inbred BXA strains in which no correlation was observed between these variables. Furthermore, insulin sensitivity and body weight correlated differently in the two backcross groups, suggesting that insulin resistance is not simply a function of obesity. The number of genes that predominantly influence diabetic traits was estimated by comparing the variance observed in (BL/6 X A/J) F1 X BL/6 backcross mice with that observed in parental mice. The data suggest that relatively few genes predominantly affect the diabetic phenotype in this murine model.
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PMID:Control of expression of insulin resistance and hyperglycemia by different genetic factors in diabetic C57BL/6J mice. 201 77

The possible alterations of zinc and copper serum levels in dyslipemies were studied. The population were classified taking into account total cholesterol HDL and triglycerides levels and the serum test at 4 degrees C in 4 groups: 1) Hypercholesterolemia (type II A), 2) Endogenous hyperlipemia (types II B and IV), 3) Mixed hyperlipemia (type V), 4) Exogenous hyperlipemia (Type I), and also the presence of over weight ("15% ideal weight body, according to Bray), that occurred in the 29.5% of the sample. Zinc and copper were determined by AAS (Smith & Butrimovitz method). Total cholesterol, HDL, LDL and triglycerides by enzymatic methods. The main results and conclusions obtained were the following: A significative increase in zinc serum level was observed; Hyperglycemia, present in nearly half of the studied population could be the responsible for it. Obesity was associated with an increase of zinc values, and this could be related to an insulinic dysfunction. A direct correlation between glycemia and triglyceridemia, and between glycemia and zincemia was found. Cardiovascular alterations seemed to decrease zinc serum levels; on the opposite however hypertension increased them. Neither lipidic metabolism alterations, nor obesity did modify copper serum level.
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PMID:[Study of zinc and copper serum levels in dislipemias]. 202 Sep 19

In order to investigate the regulation of glucose transporter gene expression in the altered metabolic conditions of obesity and diabetes, we have measured mRNA levels encoding GLUT2 in the liver and GLUT4 in the gastrocnemius muscle from various insulin resistant animal models, including Zucker fatty, Wistar fatty, and streptozocin(STZ)-treated diabetic rats. Northern blot analysis revealed that GLUT2 mRNA levels were significantly (P less than 0.001) elevated in 14 wk Zucker fatty and Wistar fatty rats relative to lean littermates but were similar in these two groups at 5 wk of age. Furthermore, there was significant increase (P less than 0.01) in GLUT2 mRNA levels in STZ diabetic rats at 3 wk after treatment. GLUT4 mRNA levels were not significantly different between control and insulin resistant rats in all animal models. These results indicate that neither hyperinsulinemia nor hyperglycemia affects GLUT4 mRNA levels in the muscle. However, GLUT2 mRNA levels in the liver were elevated in obesity and diabetes, although this regulatory event occurred independently from circulating insulin or glucose concentrations.
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PMID:Liver and muscle-fat type glucose transporter gene expression in obese and diabetic rats. 202 68

Coronary heart disease (CHD) is the major cause of mortality in the elderly. Important risk factors include hypercholesterolemia, systolic and diastolic hypertension, cigarette smoking, hyperglycemia, and obesity. Elderly patients with existing CHD should be treated aggressively to control these risk factors, along with other medical therapies to treat myocardial ischemia. For elderly patients without recognized CHD, however, a more conservative approach is recommended and includes behavioral interventions when appropriate and pharmacologic therapy for higher risk patients with persistent, uncontrolled risk factors.
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PMID:Preventive maintenance of the aging heart. 206 Aug

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

Poorly-controlled type I diabetic patients have elevated rates of leucine appearance (indicating increased proteolysis), which are reduced with insulin therapy. It also has been suggested that obesity increases leucine appearance rate by reducing sensitivity to insulin. In the present study, we examined whether non-diabetic obese women or poorly-controlled obese type II diabetic patients have elevated leucine appearance rates, and whether diabetic patients have a reduction in leucine appearance with treatment of their hyperglycemia. Among non-diabetic women, postabsorptive leucine appearance rate was positively correlated with the percentage of body weight as fat (r = 0.92, P less than 0.01). Obese women with untreated type II diabetes did not have a higher mean (+/- s.e.m.) leucine appearance rate (2.13 +/- 0.18 mumols/min/kg fat-free mass, determined by infusion of 1-[1-13C] leucine as a tracer) than obese non-diabetic women with a similar fat-free mass (2.49 +/- 0.09 mumols/min/kg fat-free mass). After two weeks of glyburide therapy mean glucose concentrations decreased 24 percent and glucose production decreased 18 percent, but leucine appearance rate was not altered (2.08 +/- 0.18 mumols/min/kg fat-free mass). After 2 weeks of insulin therapy, mean fasting glucose concentration and glucose production rate were normal (55 per cent and 46 per cent below pre-treatment levels), but leucine appearance rates remained unchanged (2.17 +/- 0.18 mumols/min/kg fat-free mass). We conclude that type II diabetes in obese patients is not associated with elevated proteolysis, that treatments that significantly improve or normalize postabsorptive glucose metabolism in obese type II diabetic patients do not affect postabsorptive proteolysis, and that obesity per se (without diabetes) increases proteolysis.
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PMID:Failure of glyburide and insulin treatment to decrease leucine flux in obese type II diabetic patients. 212 56

Insulin resistance is a cause for morning hyperglycemia seen in diabetic patients. Other reasons for morning hyperglycemia should be eliminated by performing an insulin response test. Once insulin resistance has been established as the cause of hyperglycemia, a step-by-step process should be used to establish the cause of the insulin resistance. Common causes of insulin resistance include hyperadrenocorticism, acromegaly, hyperthyroidism, and obesity. Hepatic disease, renal insufficiency, and sepsis are other causes of insulin resistance in practice. Less common causes include insulin antibodies, pregnancy, neoplasia, hyperandrogenism, and pheochromocytoma. If the underlying cause cannot be found or resolved, then increased doses of insulin are required to manage the hyperglycemia.
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PMID:Problems in diabetes mellitus management. Insulin resistance. 213 77

The risk factors vascular disease, smoking, alcohol, a diet high in saturated fat and cholesterol, sedentary life style, obesity, glucose intolerance and diabetes, high salt intake, oral contraceptives, left ventricular disease, hyperlipidemia, hyperfibrinogenemia, and uricemia are discussed in terms of evidence for added risk to hypertensive patients. Most of these risk factors have been extensively studied as contributors to the vascular diseases of the heart, brain and peripheral circulation, but not specifically in hypertensive people. For example, there is definite evidence that women with high blood pressure are at risk for coronary heart disease, and that oral contraceptives may raise blood pressure, but there are not large studies examining the level of risk for vascular disease for hypertensive women who take the pill. Similarly, the vascular risks to women who smoke and use orals are known to be multiplied, but one can only assume that hypertensive women smokers who contemplate using the pill would be at even higher risk. An exception is exercise, which has been shown to be as effective as drug therapy in lowering blood pressure and other cardiac risk factors. Generally many of these risk factors interact in a logarithmic, rather than additive manner. Furthermore, these risk factors tend to occur together more frequently in the same patient with high blood pressure more than they do in the normotensive population. High blood pressure is itself an independent risk factor for vascular disease, in proportion to its height, for all ages and sexes, whether systolic or diastolic, labile or fixed, and the threat is further aggravated by surges in blood pressure throughout the person's daily activities. In pharmacologic management of hypertension, it is important to ensure that the drug chosen does not aggravate other risk factors, such as hyperglycemia, cardiac arrhythmias or mobilization of uric acid.
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PMID:Management of vascular risk factors in the hypertensive patient. 214 91

The diabetes-associated changes in tissue norepinephrine (NE) concentrations and related adrenergic receptor types were correlated with changes in blood glucose and serum insulin levels in 8- to 16-week-old C57BL/KsJ-db/db mice relative to corresponding age-matched control (+/?) parameters. In addition, the ability of estradiol and progesterone treatments to modify the diabetes-related adrenergic imbalance was investigated. Tissue (i.e., ovarian, uterine, pancreatic, and adrenal) NE levels were determined by high-performance liquid chromatography and compared with the associated changes in tissue alpha 1,2 and beta-adrenergic membrane receptor populations. All db/db mice exhibited overt hyperglycemia, hyperinsulinemia, and obesity relative to controls between 8 and 16 weeks of age. Tissue NE levels in diabetics were either similar to, or elevated, as compared with those of age-matched controls. Although the alpha 1 and beta receptor populations (except liver) were similar in 16-week-old groups, alpha 2 receptor populations in db/db mice were elevated relative to controls. Chronic estradiol therapy effectively counteracted the diabetes-induced elevations in tissue NE and influenced all adrenergic receptor populations, normalizing both parameters to control levels as well as modifying the hyperglycemia, but not the hyperinsulinemic component, of the diabetes-obesity syndrome in this species. Chronic progesterone treatment was found to be less effective in modulating these systemic and adrenergic parameters in diabetics relative to oil- or estradiol-treated mice. These data demonstrate that a marked modification in tissue adrenergic parameters occur in association with the overt expression of the diabetes mutation in this species. The ability of estradiol treatment to normalize both blood glucose levels and tissue adrenergic parameters in C57BL/KsJ-db/db mice indicates that a direct association between systemic and cellular counter-regulating influences, relative to the severity of the Type II diabetic condition, exists in this species. The therapeutic correction of these metabolic problems by ovarian steroid hormones suggests the existence of a causal relationship between cellular glucose homeostasis and steroid action in the diabetic model.
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PMID:The effects of estradiol and progesterone on reproductive tract atrophy and tissue adrenergic indices in diabetic C57BL/KsJ mice. 215 78

Reports of an increased incidence of wound complications in surgical patients with diabetes mellitus may actually reflect the increased incidence of general surgical risks or metabolic abnormalities associated with diabetes mellitus. Factors such as age, obesity, malnutrition, and macrovascular and microvascular disease may contribute to wound infection and delayed wound healing especially in the type II diabetic patient. In addition, hyperglycemia caused by decreased insulin availability and increased resistance to insulin can affect the cellular response to tissue injury. Studies of the immune cells necessary for wound healing, such as PMN leukocytes and fibroblasts, as well as studies of injured tissue suggest that there is a delayed response to injury and impaired functioning of immune cells in diabetes mellitus. There is evidence that these impairments may be the result of both an inherent (genetic) defect as well as decreased insulin availability and increased blood glucose concentration. At the time of hospital admission, little can be done to affect most of the risk factors or inherent cellular defects. However, blood glucose levels can be controlled with the use of bedside blood glucose monitoring and frequent adjustment of insulin dosing. Nurses have traditionally played an important role in monitoring recovery from surgery and watching for signs of infection and wound complications. These nursing functions are especially important in the diabetic patient. In addition, frequent evaluation of the effectiveness of insulin therapy is an important nursing function throughout the perioperative period. Through improving management of blood glucose levels in surgical patients, nurses can have a major impact on the incidence of wound complications in diabetes mellitus.
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PMID:Wound healing in the patient with diabetes mellitus. 217 91


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