Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to clarify the mechanism of lipid metabolism during pregnancy, alpha 1-acid glycoprotein (alpha 1-AG) was analyzed in normal and diabetic pregnant women. Seventy-two determinations of serum alpha 1-AG levels were performed in 18 diabetic pregnant women and 82 determinations in 82 normal pregnant women in all three trimesters and within 14 days postpartum. Serum alpha 1-AG levels in both normal and diabetic pregnant women decreased throughout pregnancy and rapidly increased postpartum. In all gestational stages, the serum alpha 1-AG levels were lower in diabetic women than in normal women, but the differences were not significant. No significant correlation was obtained between serum alpha 1-AG and hemoglobin A1 (HbA1) in diabetic patients. On the contrary, the serum triglyceride levels increased during pregnancy and decreased postpartum in both groups of subjects. These findings suggest that serum alpha 1-AG plays an important role in the activation of lipoprotein lipase during pregnancy.
Diabetes Res Clin Pract 1990 Oct
PMID:Quantitative analysis of serum alpha 1-acid glycoprotein levels in normal and diabetic pregnancy. 226 50

Because the apparent reduction in cardiovascular risk noted in nondiabetic populations that ingest diets rich in marine lipids containing omega-3 fatty acids is believed to result in part from their capacity to modify the composition and physicochemical behavior of lipoproteins, we sought to determine whether dietary supplementation with marine lipids might favorably affect lipoprotein composition in insulin-dependent diabetes mellitus (IDDM). Eight normolipidemic IDDM women (mean +/- SD age 29.8 +/- 4.7 yr) were studied before and 3 mo after receiving a marine-lipid concentrate (Super-EPA) containing 6 g omega-3 fatty acids and a total of 12 mg of cholesterol daily. Weight, insulin requirements, and glycosylated hemoglobin remained stable. After treatment, mean +/- SD plasma triglyceride (TG) levels fell (before, 81.7 +/- 22 mg/dl; after, 69.19 +/- 17; P less than 0.025). High-density lipoprotein2 (HDL2) cholesterol (before, 10.98 +/- 5.45 mg/dl; after, 18.43 +/- 7.93; P less than 0.01), its major apolipoprotein A-I (apoAI), and the major phospholipids (sphingomyelin and lecithin) all rose significantly. ApoB and plasma and low-density lipoprotein cholesterol levels and HDL3 composition were unchanged. Postheparin hepatic and lipoprotein lipase activities were unaffected by marine lipids. These data indicate that women with IDDM experience apparently beneficial effects on TG and HDL2 from dietary supplementation with omega-3 fatty acids administered in a low-cholesterol-containing oil without adversely affecting overall diabetes management. If these changes in lipoprotein concentration and composition prove to have antiatherogenic consequences and are free of long-term toxicity, these agents may have a role in the therapy of IDDM patients.
Diabetes 1990 Apr
PMID:Effects of omega-3 fish oils on plasma lipids, lipoprotein composition, and postheparin lipoprotein lipase in women with IDDM. 231 45

Rat VLDL were glycated in vitro in the presence or absence of a reducing agent. Prior to glycation, the VLDL triglyceride was endogenously radiolabelled with [3H]-oleic acid. Post glycation the VLDL B-apoprotein was exogenously radiolabelled with [131]I. The double labelled VLDL was then injected into normal rats and the decline in plasma radioactivity of the two isotopes was used as a measure of triglyceride and particle clearance. VLDL glycated in either the presence or absence of reducing agent exhibited a significantly slower removal of triglyceride and apoprotein B compared to normal VLDL. The ability of glycated VLDL triglyceride to act as substrate for lipoprotein lipase and hepatic lipase was examined. Increasing concentrations of normal and glycated VLDL triglyceride were incubated with post-heparin plasma. The kinetics of triglyceride hydrolysis were determined in a manner analogous to Michaelis-Menten analysis. Glycated VLDL was found to be poorer than normal VLDL as a substrate for lipoprotein lipase. Glycation of VLDL appears to interfere with the lipolysis of its triglyceride. This may explain the delayed clearance of glycated VLDL triglyceride in vivo. Glycation also extended the mean plasma residence time of the VLDL particle. These factors may, in part, contribute to the hypertriglyceridaemia observed in subjects with diabetes mellitus.
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PMID:Glycation of very low density lipoprotein from rat plasma impairs its catabolism. 237 65

Primary cultures of microvascular endothelial cells and isolated adipocytes were prepared from human omental adipose tissue to study the potentially overlapping roles of insulin and insulinlike growth factors (IGFs) in human adipose tissue. To determine whether adipocytes contain type I IGF receptors, binding experiments were carried out with 125I-labeled IGF-I. At 16 degrees C, saturation of specific binding to adipocytes was reached after 30 min and was 0.7% per 10(6) cells. At 37 degrees C, chloroquine produced an increase in cell-associated 125I-IGF-I, suggesting that IGF-I is internalized and degraded in a manner analogous to insulin. In competition experiments, IGF-I competed for binding more effectively than rat IGF-II or insulin. The concentrations of IGF-I, rat IGF-II, and insulin necessary to displace 50% of 125I-IGF-I binding were 2.5, 15, and 90 nM, respectively. In addition, a monoclonal antibody (alpha-IR3) that has been shown to block the type I IGF receptor was used in competition binding experiments. The antibody also inhibited binding of 125I-IGF-I to adipocytes. The biological effects of insulin and IGF-I were examined by studying adipocyte lipoprotein lipase (LPL). Insulin stimulated [14C]glucose incorporation into cellular lipid in a dose-dependent manner, with 50% effective concentration (EC50) of 0.3 nM. However, an increase in LPL activity was observed only at a high insulin concentration, with an EC50 of approximately 30 nM. In contrast, IGF-I stimulated a progressive increase in LPL, with an EC50 of 3.2 nM. In addition, alpha-IR3 blocked the stimulatory effect of IGF-I on adipocyte LPL.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1989 Jun
PMID:Insulinlike growth factor action and production in adipocytes and endothelial cells from human adipose tissue. 254 8

Milk volume and composition were examined in a diabetic mother on days 3-7 postpartum. By day 5 milk volume produced and concentrations of sodium, potassium, chloride, lactose, protein, calcium, magnesium, and citrate were within limits of a reference population. Fat content of the milk was slightly lower. Free fatty acids were 2% of total lipid on day 3 but increased to 23% on days 4-7, suggesting impaired esterification in the mammary gland. Total milk lipoprotein lipase increased approximately fourfold during days 4-5. Other changes were 1) low cholesterol content, only one-fifth of normal milk; 2) decreased medium-chain fatty acids, suggesting impairment of fatty acid synthesis in the mammary gland; 3) increased oleic acid; and 4) high concentrations of polyunsaturated fatty acids, suggesting increased chain elongation. These results suggest that diabetes produces changes in lipid metabolism in the mammary gland that alter the composition of milk produced by the diabetic mother.
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PMID:Milk composition and volume during the onset of lactation in a diabetic mother. 259 26

The modulating effects of estradiol (E: 1 microgram/3.5 days) and progesterone (P: 2 mg/3.5 days) on the obesity and hyperinsulinemic and hyperglycemic components of the diabetes-obesity syndrome in female C57BL/KsJ (db/db) mice, which includes cellular atrophy and adiposity in the reproductive tract, were examined and compared to corresponding control (+/?) parameters. All control and diabetic mice received oil (vehicle control), E, or P treatments starting at 4 weeks of age. Body weight, serum insulin levels, blood glucose concentrations, and utero-ovarian lipoprotein lipase activities were analyzed at 8 and 16 weeks of age and related to the ultrastructural changes in the steroid-sensitive uterine epithelium during the treatment period. Neither E nor P had any effect on body weights in (+/?) or (db/db) mice. The pronounced diabetes-associated elevation in serum insulin levels was enhanced by E, and suppressed by P, in 16-week-old (db/db) mice as compared with controls. By 16 weeks of age, the E therapy normalized blood glucose levels in diabetic mice to control levels, whereas P was ineffective in modulating the hyperglycemia. The reduction in blood glucose levels in E-treated diabetic mice correlated temporally with the return of normal intracellular structure including the disappearance of intracellular lipid vacuoles characteristic of uterine epithelium cells of (db/db) mice. The diabetes-induced rise in utero-ovarian lipoprotein lipase activity was normalized by P-therapy. The reduction in utero-ovarian lipoprotein lipase activity coincided temporally with the demonstrated intracellular reorganization in (db/db) reproductive tract tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of estradiol and progesterone on diabetes-associated utero-ovarian atrophy in C57BL/KsJ (db/db) mutant mice. 268 92

In 21 non-insulin-dependent diabetic patients with secondary drug failure, once-daily long-acting insulin lead to a moderately improved metabolic control. At the conclusion of the study (eight months) the fasting blood glucose and HbA1c concentrations were significantly decreased, but the postprandial blood glucose concentrations in the afternoon were unaltered. The peripheral insulin sensitivity, as measured by the intravenous insulin tolerance test, and the lipoprotein lipase activity in adipose and skeletal muscle tissue had increased. After initiation of insulin therapy there was a transient decrease of the fasting and glucagon-stimulated C-peptide concentrations. The very low density lipoprotein lipids and apolipoprotein B, A-I and A-II were also reduced transiently. The only significant difference in lipoprotein composition at eight months compared with on admission, was an increased cholesterol and decreased triglyceride concentration in the high density lipoproteins. There were significant relationships between the C-peptide, but not the peripheral insulin, concentrations and the serum lipid concentrations. This may indicate that high peripheral insulin concentrations after administration of exogenous insulin may affect the hepatic lipoprotein production less than the portal insulin concentrations mainly derived from endogenous production.
Diabetes Res 1989 Nov
PMID:C-peptide but not insulin concentrations are related to the serum lipoprotein levels during insulin treatment of non-insulin-dependent diabetes mellitus (NIDDM) patients. 269 85

The sand rat (Psammomys obesus) is a desert rodent in which obesity and diabetes mellitus appeared only subsequent to feeding laboratory animal chow. To study the role of lipoprotein lipase in the development and maintenance of obesity in the sand rat, enzyme activity in various organs and in plasma of sand rats or albino rats was determined following a 20-hour fast, or 16 hours after injection of cholera toxin. Despite comparable change in body weight, an altered pattern of enzyme distribution and regulation was observed in the sand rat. Neither fasting nor cholera toxin had an effect on heart and daiphragm muscle lipoprotein lipase activity of the sand rat, but caused a 1.5- to 2-fold increase in the treated albino rats. By using an isolated perfused heart system, we were able to measure enzyme activity present in the heparin-releasable fraction that represents the functional pool of the enzyme. In both species, the heparin-releasable fraction of the heart increased twofold following fasting, though initial values were lower in sand rat. In both species, fasting and cholera toxin administration resulted in an increase in plasma and liver lipoprotein lipase activity. Adipose tissue lipoprotein lipase activity of sand rat, unlike the albino rats, was similar in the various fat regions and was not lowered by food deprivation or cholera toxin administration. After both treatments, sand rat plasma insulin levels exceeded fivefold those of albino rats. Adipose tissue lipoprotein lipase activity of fed and fasted normal and diabetic sand rats correlated negatively with plasma insulin and glucose levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of lipoprotein lipase activity in the sand rat: effect of nutritional state and cAMP modulation. 284 76

The relationship between erythrocyte membrane structural and functional alterations and plasma lipids was studied in three patients with chylomicronemia due to either lipoprotein lipase (LPL) deficiency, apo C-II deficiency (in an individual who also suffers from thalassemia minor) or coexistent diabetes mellitus (and decreased LPL activity) and in a patient with Tangier disease. All of the patients' erythrocytes had significantly elevated phosphatidyl-choline (PC): sphingomyelin (Sph) ratios (most marked in the patient with Tangier disease). Major differences were observed in the PC: Sph ratios of erythrocytes and plasma. The pattern of changes in erythrocyte membrane enzyme activities differed despite similarities in the lipid composition of the erythrocytes. The changes in osmotic fragility (OF) were inversely related to the membrane cholesterol:phospholipid ratio. An even stronger negative correlation was found between OF at the lowest NaCl concentrations and the activities of both Na+,K+- and Mg++-ATPases. The ratio of total: surface sulfhydryl titres also correlated significantly with OF.
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PMID:Erythrocyte membrane alterations and plasma lipids in patients with chylomicronemia and in Tangier disease. 301 88

Severely hyperlipidemic alloxan-diabetic cholesterol-fed rabbits were treated with different daily doses of insulin in order to study the effect of insulin on plasma lipids, lipoproteins and postheparin lipoprotein lipase activity. At plasma triglyceride levels of 15,000 mg/dl, untreated diabetic rabbits carried 73% (1950 mg/dl) of plasma total cholesterol in lipoproteins with a diameter larger than 75 nm (Sf greater than 400), 25% in smaller very low density lipoproteins (VLDL) and 1% in both low and high density lipoproteins (LDL, HDL). Insulin treatment greatly reduced plasma total cholesterol and triglyceride concentrations. The decrease of plasma total cholesterol concentration was paralleled by a decrease in the cholesterol of the largest lipoproteins (Sf greater than 400) and an increase in cholesterol of both smaller very low density lipoproteins and low density lipoproteins. At the same time, postheparin plasma lipoprotein lipase activity increased 2-8-fold. When plasma triglyceride levels were normalized by insulin treatment, the lipoprotein cholesterol distribution in diabetic cholesterol-fed rabbits was similar to that of normal cholesterol-fed rabbits. To study development of atherosclerosis, diabetic rabbits were cholesterol-fed and treated with insulin for eight weeks such that the triglyceride levels were normalized, but plasma glucose levels were still greatly elevated. Nondiabetic rabbits were cholesterol-fed simultaneously. Plasma cholesterol and triglyceride levels were similar in the two groups of rabbits, as well as cholesterol in Sf greater than 400 or smaller VLDL and cholesterol in HDL. However, LDL-cholesterol concentration in the insulin-treated diabetic rabbits was 1.5-2 times that in the nondiabetic rabbits. The two groups of rabbits developed similar degrees of atherosclerosis, as judged by aortic cholesterol content. Apparently, partially controlled diabetes in cholesterol-fed rabbits does not accelerate atherogenesis beyond that observed in nondiabetic cholesterol-fed rabbits.
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PMID:Hyperglycemia in normotriglyceridemic, hypercholesterolemic insulin-treated diabetic rabbits does not accelerate atherogenesis. 306 65


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