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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas. Twelve young, healthy men were given 1 g of tolbutamide by mouth before and after 12 days of double-blind treatment with 1 g per day of halofenate, or placebo. There was a significant increase in serum tolbutamide at eight, 10 and 12 hours (P less than 0.01) and a significant (P less than 0.01) decrease in serum glucose at one, four and six hours after halofenate treatment, but not after placebo. In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both. No appreciable decrease in serum glucose levels was noted in diabetic patients receiving sulfonylurea and clofibrate. This interaction between halofenate and sulfonylureas is clinically important, especially in view of the association of hyperlipemia and diabetes.
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PMID:Potentiation of hypoglycemic effect of sulfonylureas by halofenate. 17 74

Metformin's hypolipidemic effects (2.55 g/day for 3 months) have been studied in 19 subjects with Fredrickson's Type IV hyperprebetalipoproteinemia. The majority of patients were above ideal body weight (relative body weight = 118 +/- 2.7 %). Eleven of the subjects presented chemical diabetes, 5 fasting hyperglycemia, and 3 normal glucose tolerance. After treatment with metformin, body weight showed a slight, but significant reduction (--2.4 +/- 0.3 kg). Glucose tolerence was not substantially altered while basal glucose was significantly reduced in the 5 subjects with fasting hyperglycemia. Basal plasma insulin was significantly reduced in all the patients following metformin treatment. Insulin response to OGTT was slightly reduced in the subjects with fasting hyperglycemia. Independent of the patients' glucose tolerance, metformin treatment induced a marked decrease in plasma triglycerides (-- 40 %) and a reduction in plasma cholesterol (-- 12 %). No correlation was found between triglyceride and cholesterol reduction and body weight, glucose, and plasma insulin variations. Like phenformin, metformin acts not only on glucose metabolism and insulin secretion but on lipid metabolism as well.
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PMID:Hypolipidemic effects of metformin in hyperprebetalipoproteinemia. 18 98

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
Diabetes 1978 Jun
PMID:Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. 65 14

The nature of Type V hyperlipoproteinemia including mode of presentation, prominent clinical and biochemical features, and genetics, was examined in 29 adults presenting with the Type V lipoprotein phenotype. Initially 23 of the 29 patients had various metabolic stimuli (diabetes out of control, estrogenic agents, pancreatitis, ethanolism) superposed on their acute hypertriglyceridemia. After metabolic stabilization, 17 of the 29 subjects were shown to have familial hypertriglyceridemia. In the 17 kindreds with familial hypertriglyceridemia, the lack of a specific, distinctive genetic marker for the Type V genotype and for the Type IV genotype restricts the conclusion that the pattern of inheritance was consistent with an autosomal dominant trait.
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PMID:Familial and acquired type V hyperlipoproteinemia. 107 94

Among 91 index cases whose diagnosis of a genetic type of hypertriglyceridemia was based on family studies, 27% had diabetes. To determine whether the familial forms of hypertriglyceridemia and genetic diabetes mellitus are inherited together or independently, the adult first degree relatives of these propositi were investigated for the presence of diabetes. Frequency of diabetes in first degree relatives of the 25 diabetic patients with a familial form of hypertriglyceridemia was identical whether such relatives were hyperlipidemic or not (13% versus 14.7%). The frequency of diabetes in both the hyperlipidemic and normolipidemic relatives of the 66 nondiabetic hypertriglyceridemic index cases also was not significantly different from each other (6.2% versus 4.0%). These results indicate that while diabetes is frequently associated with hypertriglyceridemia, genetic hypertriglyceridemia, per se, does not carry an increased risk of diabetes. Following treatment of diabetes, elevated triglyceride levels in index cases with both familial hypertriglyceridemia and untreated diabetes returned to lower but still elevated levels resembling those of affected (hypertriglyceridemic) relatives. Thus, the interaction of untreated diabetes and a familial form of hypertriglyceridemia determines the level of plasma triglyceride in a patient with both disorders.
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PMID:Evidence for diabetes mellitus and genetic forms of hypertriglyceridemia as independent entities. 116 27

Primary familial forms of chylomicronemia can lead to acute life-threatening complications, especially acute pancreatitis. The main aim of therapy is to avoid this so-called chylomicronemia syndrome. In 12 patients with primary chylomicronemia due to familial hypertriglyceridemia, the addition of 2.16 g omega-3 fatty acids over 4 weeks and 4.32 g for 8 weeks resulted in a decrease of serum triglyceride levels from 1,624 +/- 333 to 894 +/- 241 mg/dL after 12 weeks. Cholesterol and triglyceride levels in the chylomicron fraction were reduced concomitantly, the apolipoprotein B-100/B-48 ratio increased, very--low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol, and total cholesterol levels decreased, and low-density lipoprotein (LDL) cholesterol showed a tendency to increase, but this finding did not reach significance. High-density lipoprotein (HDL) cholesterol levels remained unchanged, as did the levels of apolipoproteins A-I, A-II, and E, and lipoprotein(a). Apolipoprotein B levels decreased significantly. The decrease of triglyceride levels to still-elevated concentrations was accompanied by a substantial decrease in plasma and whole-blood viscosity and erythrocyte aggregation, which reached normal values. As in chylomicronemia, complications usually occur at triglyceride levels higher than 1,500 mg/dL; patients can still profit from treatment with omega-3 fatty acids, even though triglyceride levels are still substantially elevated. No clinically relevant side effects occurred, with the exception of the manifestation of diabetes mellitus in one patient, which could be reversed after discontinuation of treatment.
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PMID:Treatment of primary chylomicronemia due to familial hypertriglyceridemia by omega-3 fatty acids. 140 95

Hypertriglyceridemia is not a common finding in well controlled patients with insulin dependent diabetes; however, in noninsulin dependent, or Type II diabetes, hypertriglyceridemia and coronary heart disease are a well recognized clinical triad. In the latter setting, hypertriglyceridemia is usually the result of an associated inherited hyperlipidemia, most commonly familial hypertriglyceridemia but also familial combined hyperlipidemia. In the former, one sees elevated triglycerides and a low HDL-cholesterol, in the latter the same phenotype may be present but often there is a high LDL-cholesterol. Irrespective of the pathogenesis of the primary hypertriglyceridemic disorder, the occurrence of poorly controlled diabetes will enhance the hypertriglyceridemia and even in the Type II diabetic, with triglycerides in the thousands, dietary and glycemic control, alone, will strikingly ameliorate the hypertriglyceridemia. In contrast to patients with hypercholesterolemia, no national guidelines have been proposed for the treatment of patients with hypertriglyceridemia. Yet both experimental and clinical data support an algorithm in which dietary and glycemic control are optimized with a resultant major improvement in triglycerides, followed by the introduction of drug therapy. Three agents are particularly useful in correcting the hypertriglyceridemia: gemfibrozil, niacin, and fish oils, with the first two having the added benefit of increasing HDL levels. Lovastatin is also useful in treating these patients, but primarily for lowering LDL-cholesterol while triglycerides are independently being brought under control. Correction of hyperlipidemia in diabetic patients can generally be achieved with judicious use of dietary, glycemic and drug therapy; however, maintenance of a favorable response requires a high level of patient compliance, which is usually difficult to sustain.
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PMID:Hypertriglyceridemia in diabetes. An approach to management. 176 54

In order to learn whether patients with diabetic ketosis who had very severe hypertriglyceridemia had underlying genetic hyperlipidemia, the authors measured plasma lipids in 211 episodes. They report the findings in the 15 patients who had initial plasma triglyceride concentrations above 11.3 mmol/L (1,000 mg/dL). These patients were detected during a prospective study of 155 episodes of ketoacidosis and 56 episodes of ketosis. Eleven of the 15 patients had definite or probable insulin-dependent diabetes mellitus (IDDM), but eight of the 15 were not acidemic despite their ketosis. Twelve of the 15 patients (80%) were men, a far higher percentage of men than the 53.6% in the base population of 211 episodes. Plasma triglyceride concentrations returned to normal levels either during the acute episode (seven cases) or well within a year (two more cases) in most of the patients. From that and other considerations, the authors infer that at least ten, and perhaps 12 of the 15 patients did not have an underlying genetic hyperlipidemia contributing to their original severe hypertriglyceridemia. That contrasts with the findings of others who reported that most patients with severe hypertriglyceridemia associated with noninsulin-dependent diabetes mellitus (NIDDM) (usually without ketosis) did have coexisting familial hypertriglyceridemia.
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PMID:Severe hypertriglyceridemia in diabetic ketosis. 212 81

We report on clinical and metabolic studies of a newly delineated lipomatosis, characterised by an abnormal mediastinal and abdominal accumulation of fat, without obesity. The clinical features, which occurred in all the patients studied, are: Exertional dyspnoea due to a space-occupying mediastinal accumulation of fat, without evidence of cardiac or pulmonary disease. A pseudo-ascitic abdominal enlargement, due to intra- and retroperitoneal accumulation of fatty tissue. Insulin-independent diabetes mellitus. Type IV hyperlipidaemia and elevated levels of plasma uric acid were observed in four patients. Intra-abdominal lipomatous tissue, obtained during laparoscopy from four patients, demonstrated a reduced lipolytic response to beta-adrenergic stimulation. Thus, fat deposition in the abdominal and mediastinal areas could be causally related to defective lipid mobilization in lipomatocytes. Lipoprotein lipase activity in abdominal adipose tissue were normal in two patients (10.0 and 10.6 nmol/g/min) and markedly elevated in another two patients (37.3 and 49.9 nmol/g/min), as compared with controls (12.7 +/- 2.1 nmol/g/min). When expressed on per cell basis, LPL activity in lipomatous tissue was significantly higher than in control tissue (3.21 +/- 1.1 nmol/10(5) cell/min vs 0.92 +/- 0.16 nmol/10(5) cell/min). Lipoprotein fractionation did not demonstrate consistent modification of the serum lipoprotein pattern. HDL and HDL2 cholesterol values were reduced, even in patients with elevated LPL activity in adipose tissue.
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PMID:Mediastino-abdominal lipomatosis: deep accumulation of fat mimicking a respiratory disease and ascites. Clinical aspects and metabolic studies in vitro. 651 1

Hyperlipoproteinemia occurs commonly in diabetics and may contribute to early atherosclerosis in these patients. The effect of dietary carbohydrate restriction on lipid abnormalities has been examined in 42 newly diagnosed maturity-onset diabetics, in whom plasma lipoproteins were measured before treatment was started and at regular intervals during ten months of dietary therapy. Twenty-four patients (57%) had abnormal lipids when diabetes was first diagnosed. Nine were classed as Type II and 15 as Type IV hyperlipoproteinemia. Plasma lipids reverted to normal in half these patients after dietary treatment for one month. Only 8 diabetics (19%) showed persistent lipid abnormality after ten months' treatment: all had been unable to diet satisfactorily as judged by persisting obesity and hyperglycemia. The common lipoprotein abnormalities of maturity-onset diabetes can usually be returned to normal by the simplest possible carbohydrate-restricted diet, if patients adhere to this. Specialized and complex diets or lipid-lowering drugs are unncessary in the majority of patients.
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PMID:Effect of carbohydrate restriction on lipoprotein abnormalities in maturity-onset diabetes mellitus. 741 53


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