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

A successful GnRH treatment for hypogonadotropic hypogonadism is described. A 40 year old infertile patient due to Kallmann's syndrome, associated with obesity and NIDDM, was treated with HCG (5,000 IU/week) for 8 years. In an attempt to induce spermatogenesis HMG (75 IU/daily) was added for 2 years. During the combined gonadotropin treatment semen analysis indicated an improvement from azoospermia to 2 x 10(6) sperm/ml. Since semen quality remained poor and obviously no pregnancy was achieved, the last regime was replaced by a pulsatile GnRH treatment (5 mcg/90 minutes). Following 6 months sperm count increased up to 15 x 10(6) associated with normal motility and morphology. Patient's wife conceived after the second intrauterine insemination and delivered a full term healthy baby.
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PMID:Successful GnRH treatment in a patient with Kallmann's syndrome, who previously failed HMG/HCG treatment. 314 74

Non-insulin-dependent diabetes (NIDDM) is a major cause of premature morbidity and mortality among adults. Macrovascular disease of coronary and peripheral vessels is the primary cause of death in these patients. Numerous experimental and epidemiologic studies have suggested that hyperinsulinemia accelerates the development of atherosclerosis. In experimental models, insulin promotes diet-induced lesion development and overrides lesion regression and estrogen protection against atherosclerosis. Local hyperinsulinemia induced by selected arterial infusion accelerates atherosclerosis in the perfused artery. Insulin has been shown to stimulate subintimal smooth muscle and fibroblast cells in culture, and to increase the uptake and local synthesis of lipid by these cells. Insulin may also induce inhibition of fibrinolysis. Several prospective studies performed on nondiabetic patients show that either fasting or postprandial insulin levels are a sensitive predictor of the development of coronary disease independent of other risk factors. Two recent studies in NIDDM patients confirm this finding and suggest that glycemic control may not be a significant factor in the development of macrovascular disease. Diseases of carbohydrate tolerance, ie, NIDDM, impaired glucose tolerance, obesity, are frequently associated with elevated circulating insulin levels, either physiologically or secondary to treatment. Given the high prevalence of cardiovascular disease in these populations, modifying therapy to minimize hyperinsulinemia should be an important consideration in a treatment program. Use of oral agents such as glipizide or gliclazide, which induce less diurnal hyperinsulinemia, may be advantageous when compared to traditional oral agent or insulin therapy.
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PMID:Atherosclerosis in diabetes: the role of hyperinsulinemia. 327 13

The major obstacle to a recommendation for screening adults for NIDDM is the conflicting evidence that early detection and treatment reduce future complications. Because obesity is a risk factor for NIDDM, and hypertension in conjunction with NIDDM leads to early atherosclerosis, treatment is indicated for both hypertension and obesity whether or not NIDDM is present concurrently. It is clear that there are those who accept and those that reject the use of oral hypoglycemic agents. Accordingly, there are those who believe that the goal of NIDDM treatment is zealous glycemic control and those who are not so inclined. Whether or not to screen for NIDDM ultimately depends upon which view is adopted. While it may seem prudent to screen for and insist upon "tight" control of NIDDM, we should consider the effect of labeling asymptomatic persons from a positive test result. What are the repercussions regarding status of employment and insurance eligibility as compared to benefits of treatment? What is the psychosocial impact? Although no studies on the effect of labeling patients non-insulin-dependent diabetics could be located, a study of hypertension in an industrial setting demonstrated that patients labeled hypertensive had an increased absenteeism from work. Interestingly, the main factors associated with increased absenteeism were awareness of the condition and low compliance with treatment. Although the parallel to NIDDM is evident, additional studies are needed.
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PMID:Screening for non-insulin-dependent diabetes mellitus. 329 Sep 20

Recent studies have revealed that family functioning affects diabetic control, compliance behavior, and treatment of obesity, all of which are issues important to the care of the NIDDM patient. By assessing a few important family dynamics and intervening where appropriate, primary care physicians cannot only improve family functioning, but the health of their patients as well. Family therapy may be necessary when families are resistant to practitioner interventions.
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PMID:Functional assessment of families with a diabetic person. 329 Sep 21

This article reviews current research about the pathogenesis of obese NIDDM relevant to its dietary management. It summarizes the findings about four dietary interventions: fasting; very low-calorie diets; hypocaloric balanced-deficit diets; and variation of constituents within a diet. The review recommends a specific primary care strategy: induce an extended remission of NIDDM in the obese patient in the short-term; and treat the cause of NIDDM and the behaviors that promote obesity in the long-term with group competition programs.
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PMID:The dietary management of non-insulin-dependent diabetes mellitus in the obese patient. 329 Sep 23

Hyperinsulinaemia is of great importance, being a primary risk factor for cardiovascular disease and non-insulin dependent diabetes (NIDDM). Furthermore, unwanted effects of increased exposure of tissues to insulin are known. Hyperinsulinaemia may, in principle, be caused by primary hypersecretion, or be a secondary consequence of diminished effectiveness of insulin in the periphery. Obesity is the commonest condition characterized by insulin resistance, which is seen most frequently when excess adipose tissue is localized to the abdominal region. Insulin resistance in obesity is found in several tissues, however, with liver and muscle being quantitative the most important. Muscle insulin sensitivity is regulated by genetic factors, hormonal effects, and the influence of free fatty acids, as well as the state of physical activity. There is evidence for the action of each of these factors in obesity. The pathogenetic mechanisms linking hyperinsulinaemia with cardiovascular disease and NIDDM are unknown. Comparisons between development of NIDDM in experimental animal models and in humans in prospective studies however, provide useful hypotheses for further studies.
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PMID:Adipose tissue distribution, plasma insulin, and cardiovascular disease. 330 69

To determine the contribution of obesity to the insulin resistance of non-insulin-dependent diabetes mellitus, insulin dose response curves for suppression of glucose production and stimulation of glucose utilization were generated in lean and obese diabetic patients and compared to those observed in weight-matched nondiabetic subjects. Glucose utilization during 0.4, 1.0, and 10.0 mU/kg x min insulin infusions (producing insulin concentrations ranging from approximately 50 to 2,000 microU/mL) was lower (p less than .02 to .001) in lean and obese diabetic patients compared to weight-matched nondiabetic subjects indicating insulin resistance. Glucose utilization was not correlated with obesity in the diabetic subjects. Suppression of glucose production was impaired (P less than .03 and .001) in both the lean and obese diabetic subjects at physiologic but not supraphysiologic insulin concentrations. We conclude that patients with NIDDM have both hepatic and extrahepatic insulin resistance, the severity of which appears to be independent of the degree of obesity.
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PMID:Insulin action in non-insulin-dependent diabetes mellitus: the relationship between hepatic and extrahepatic insulin resistance and obesity. 331 38

To determine the effects of very-low-calorie diets on the metabolic abnormalities of diabetes and obesity, we have studied 10 obese, non-insulin-dependent diabetic (NIDDM) and 5 obese, nondiabetic subjects for 36 days on a metabolic ward during consumption of a liquid diet of 300 kcal/day with 30 g of protein. Rapid improvement occurred in the glycemic indices of the diabetic subjects, with mean (+/- SEM) fasting plasma glucose falling from 291 +/- 21 to 95 +/- 6 mg/dl (P less than 0.001) and total glycosylated hemoglobin from 13.1 +/- 0.7% to 8.8 +/- 0.3% (P less than 0.001) (normal reference range 5.5-8.5%). Lipid elevations were normalized with plasma triglycerides reduced to less than 100 mg/dl and total plasma cholesterol to less than 150 mg/dl in both groups. Hormonal and substrate responses were also comparable between groups with reductions in insulin and triiodothyronine and moderate elevations in blood and urinary ketoacid levels without a corresponding rise in free fatty acids. Electrolyte balance for sodium, potassium, calcium, and phosphorus was initially negative but approached equilibrium by completion of the study. Magnesium, in contrast, remained in positive balance in both groups throughout. Total nitrogen loss varied widely among all subjects, ranging from 70 to 367 g, and showed a strong positive correlation with initial lean body mass (N = 0.83, P less than 0.001) and total weight loss (N = 0.87, P less than 0.001). The nondiabetic group, which had a significantly greater initial body weight and lean body mass than the diabetic group, also had a significantly greater weight loss of 450 +/- 31 g/day compared with 308 +/- 19 g/day (P less than 0.01) in the diabetic subjects. The composition of the weight lost at completion was similar in both groups and ranged from 21.6% to 31.3% water, 3.9% to 7.8% protein, and 60.9% to 74.5% fat. The contribution of both water and protein progressively decreased and fat increased, resulting in unchanged caloric requirements during the diet. This study demonstrates that short-term treatment with a very-low-calorie diet in both obese diabetic and nondiabetic subjects results in: safe and effective weight loss associated with the normalization of elevated glucose and lipid levels, a large individual variability in total nitrogen loss determined principally by the initial lean body mass, and progressive increments in the contribution of fat to weight loss with stable caloric requirements and no evidence of a hypometabolic response.
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PMID:Metabolic consequences of very-low-calorie diet therapy in obese non-insulin-dependent diabetic and nondiabetic subjects. 351 Sep 22

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.
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PMID:Definition of diabetes mellitus. 351 69

In spite of maximal doses of sulphonylurea agents, patients with poorly controlled non-insulin dependent diabetes (NIDDM) often do not have improved metabolic control after the introduction of insulin therapy. We have assessed 22 patients with NIDDM who commenced insulin therapy in order to identify those characteristics which were associated with an improvement in glycaemic control. Twelve months after the commencement of insulin therapy, 14 (64%) patients showed a decrease in glycosylated haemoglobin (HbA1) levels; 12 of the 14 (55%) patients had achieved HbA1 levels that were considered to reflect acceptable glycaemic control (HbA1 less than or equal to 11%; reference range, 6%-9%). The HbA1 levels in the other patients either remained unchanged or had increased (one subject). When the subjects who had achieved good glycaemic control with insulin therapy were compared with the remainder of the group, a failure to improve with insulin therapy was associated with a longer duration of diabetes, greater obesity and higher levels of cholesterol and triglycerides before the commencement of insulin therapy. Greater obesity and high levels of circulating lipids were found by means of multiple linear regression analysis to correlate independently with a poor response to insulin therapy. We conclude that standard insulin therapy can improve the majority of patients with poorly controlled NIDDM. However, there is a substantial number of patients, who tend to be obese and have high levels of circulating lipids, whose condition does not improve with insulin therapy, or who require more aggressive dosage increases than are used as a routine.
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PMID:Insulin therapy in patients with poorly controlled non-insulin dependent diabetes mellitus. 354 52


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