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

The effects of four months' physical exercise on serum lipids, lipoproteins and lipid metabolizing enzymes were studied in 25 non-insulin-dependent diabetic patients divided randomly into exercise (n = 13) and control (n = 12) groups. Exercise induced a significant decrease in serum LDL-cholesterol and an increase in serum HDL-cholesterol and HDL2-cholesterol. Triglycerides showed a temporary decrease. Apoproteins A1 and B were virtually unchanged. Postheparin plasma lipoprotein lipase increased markedly during the exercise period while no change occurred in adipose tissue lipoprotein lipase, hepatic lipase or lecithin:cholesterol acyltransferase. In the control group no significant changes occurred in any of the lipid variables. In the light of the knowledge of LDL-cholesterol as a causative and HDL-cholesterol as a protective factor in atherogenesis in non-diabetics the changes caused by exercise in non-insulin-dependent diabetics can be considered favourable.
Diabetes Res 1988 Feb
PMID:Effects of long-term physical exercise on serum lipids, lipoproteins and lipid metabolizing enzymes in type 2 (non-insulin-dependent) diabetic patients. 339 67

We measured serum lipids, lipoproteins and post-heparin plasma lipases, lipoprotein lipase and hepatic lipase, in 12 female patients with Type 1 (insulin-dependent) diabetes (postglucagon C-peptide undetectable), in 11 female insulin-treated patients with Type 2 (non-insulin-dependent) diabetes (postglucagon C-peptide greater than 0.60 nmol/l) and in 16 non-diabetic female control subjects. These three groups of subjects were similar with respect to age and obesity. Insulin dose was similar in patients with Type 1 and with Type 2 diabetes. HDL and HDL2 cholesterol were lower in patients with Type 2 diabetes than in non-diabetic control subjects (p less than 0.05) but did not differ between patients with Type 1 diabetes and non-diabetic control subjects. No difference in lipoprotein lipase activity was seen between the groups. The highest levels of lipoprotein lipase and hepatic lipase activities were observed in patients with Type 2 diabetes. Lipoprotein lipase activity correlated significantly with HDL cholesterol in patients with Type 1 diabetes (p less than 0.01) and in patients with Type 2 diabetes (p less than 0.001) but not in control subjects. Hepatic lipase activity did not correlate significantly with HDL cholesterol in any of the groups. In conclusion, postheparin plasma lipoprotein lipase and hepatic lipase activities do not seem to explain the difference in HDL cholesterol concentration between patients with Type 1 and Type 2 diabetes.
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PMID:Relationship between postheparin plasma lipases and high-density lipoprotein cholesterol in different types of diabetes. 342 2

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease]. 345 43

Four-five months after the induction of diabetes, salivary tissues of male Wistar rats were preserved by glutaraldehyde fixation or rapid freezing in dry-ice cooled hexane. Fixed tissues were either processed and embedded for light and electron microscopy, or frozen and, together with unfixed tissues, sectioned and stained with Oil Red 0 or by the calcium-lipase method. All diabetic glands had considerably more intracellular lipid than control ones. Lipid accumulation within parenchymal cells varied with the type of gland, and was more pronounced in animals with the highest serum-glucose levels. Serous cells of parotid and sublingual glands accumulated the greatest amount of lipid; lesser amounts were present in seromucous acinar cells of submandibular glands; little or none in mucous acinar cells of sublingual glands. There was no lipid in striated, granular or excretory ducts. Histochemical staining suggested that the intracellular lipid was mainly triglyceride which may accumulate by increased uptake for use as an energy source, or by decreased use in the synthesis of secretory granule and plasma-membrane material.
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PMID:Lipid accumulation in the major salivary glands of streptozotocin-diabetic rats. 346 70

Exocrine and endocrine pancreatic functions were studied in 30 patients with homozygotic beta-thalassaemia. All were treated with continuous subcutaneous deferoxamine infusions for a mean period of 30 months. Three patients (aged 18-22 years) had insulin-dependent diabetes, two before and one shortly after the onset of deferoxamine administration. There was no improvement during the treatment. An abnormal glucose tolerance test was demonstrated in 14 patients (47%) before and in seven (23%) during deferoxamine infusion. Enzyme activity of alpha-amylase and lipase as an expression of exocrine pancreatic function was normal in all during the observation period. Improvement in endocrine pancreatic function was apparently age-dependent: the younger the patient at the onset of treatment the more likely is normalization of the oral glucose tolerance test.
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PMID:[Continuous subcutaneous deferoxamine infusions in thalassemia major. Improvement in glucose tolerance]. 348 6

High vitamin E supplementation in the diets of streptozocin-induced diabetic rats eliminates accumulation of lipid peroxides in the plasma and the liver, returns the plasma triglycerides toward normal levels, and increases the activity of lipoprotein lipase. Vitamin E has no effect on the levels of insulin or glucose. These findings suggest that vitamin E increases the total hepatic triglyceride lipase activity by increasing the lipoprotein lipase activity possibly by protecting the membrane-bound lipase against peroxidative damage.
Diabetes 1986 Mar
PMID:Triglyceride-lowering effect of dietary vitamin E in streptozocin-induced diabetic rats. Increased lipoprotein lipase activity in livers of diabetic rats fed high dietary vitamin E. 351 38

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.
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PMID:Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth. 352 12

To evaluate mechanisms of diabetes-induced changes in very-low-density lipoprotein (VLDL), VLDL triglyceride (TG) and VLDL apolipoprotein B (apoB) metabolism were studied in 12 obese Pima Indian control subjects and in 15 Pima Indian obese non-insulin-dependent diabetics. Eleven of the diabetics were restudied after reduction of hyperglycemia with oral sulfonylurea therapy. In addition, adipose, muscle, and postheparin lipoprotein lipase and postheparin hepatic lipase activities were measured in all subjects. Obese diabetics as compared with obese controls showed a trend toward increased production of VLDL TG (46 +/- 4 vs. 35 +/- 6 g/day, P = .10) but not of VLDL apoB (1595 +/- 106 vs. 1597 +/- 164 mg/day, NS); production of VLDL TG declined to control levels (33 +/- 4 g/day, P less than .05) during therapy, whereas there was no change in production of VLDL apoB. Diabetics had a clearance defect for VLDL, indicated by significantly lower fractional catabolic rates for both VLDL TG (10.6 +/- .9 vs. 13.1 +/- .9 pools/day, P less than .05) and VLDL apoB (5.6 +/- .4 vs. 7.5 +/- 0.7, P less than .05) as compared with controls; fractional catabolic rates increased after therapy (to 13.3 +/- 1.5, P less than .05, and 6.7 +/- .4, P less than .05, respectively). In the diabetics, this decrease in clearance was accompanied by a lower adipose lipoprotein lipase (.30 +/- .09 vs. .92 +/- .25 mumol X g-1 X h-1, P less than .01), which increased during therapy (to .61 +/- .17, P less than .05). Hepatic lipase also decreased significantly after therapy (27.4 +/- 3.6 to 26.4 +/- 3.2, P less than .01). Composition of VLDL in diabetics was also abnormal, indicated by a higher TG/apoB ratio (14.7 +/- .6 vs. 11.7 +/- .8, P less than .01); this ratio fell during therapy (to 12.5 +/- .8, P less than .05). The data indicate there are multiple abnormalities in structure and metabolism of VLDL in non-insulin-dependent diabetics. Control of hyperglycemia with sulfonylureas has the capability of reversing some of these abnormalities.
Diabetes 1986 Nov
PMID:Effects of NIDDM on very-low-density lipoprotein triglyceride and apolipoprotein B metabolism. Studies before and after sulfonylurea therapy. 353 Aug 55

There is a very high probability that lipoprotein metabolism plays a central role in the etiology of coronary heart disease. In sedentary persons one way to favorably alter lipoprotein metabolism and possibly delay the progression of coronary atherosclerosis is by an increase in their habitual physical activity. More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I. Plasma low-density lipoprotein concentrations usually are not significantly reduced by exercise unless accompanied by weight loss, but there may be important changes in the distribution among the low-density subfractions. These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase. In healthy persons as well as in patients with ischemic heart disease, diabetes and renal failure, an increase in moderate-intensity, endurance-type activity requiring an expenditure of approximately 4 MJ (1,000 kcal) per week usually produce favorable lipoprotein changes. Above this level a dose-response relationship exists, with greater changes occurring up to energy expenditures of 19 MJ (4,500 kcal) per week.
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PMID:The influence of exercise training on plasma lipids and lipoproteins in health and disease. 353 12

The placental transfer of non-esterified fatty acids, predominantly in the direction of mother to fetus, is regulated on a gross scale by the transplacental non-esterified fatty acid gradient. This is maintained by fetal liver lipid uptake and by enhanced lipolysis of circulating triacylglycerol in the pregnant mother. It is also dependent upon maternal placental blood flow, which is reduced in diabetes, upon the fetal umbilical blood flow, upon maternal and fetal albumin concentrations and upon intratrophoblastic fatty acid binding protein, which appears to be altered in diabetes. Circulating maternal triacylglycerols also directly contribute non-esterified fatty acids to the fetus by intraplacental hydrolysis and the hypertriglyceridaemia associated with maternal diabetes, in concert with changes in lipase levels will enhance maternal to fetal lipid flux.
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PMID:Placental transfer of non-esterified fatty acids in normal and diabetic pregnancy. 355 63


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