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)

Amounts of plasma lipids, apolipoprotein AI (apo AI) and apolipoprotein E (apo E) were measured in streptozotocin-induced diabetic rats. Plasma triglyceride and cholesterol levels of diabetic rats were not significantly different from those of control rats. Plasma apo AI levels of diabetic rats were significantly higher than those of control rats (78.2 +/- 29.3 vs 27.2 +/- 3.4 mg/dl, P less than 0.001), while plasma apo E levels of diabetic rats were significantly lower than those of control rats (4.2 +/- 1.0 vs 13.9 +/- 5.3 mg/dl, P less than 0.001). Insulin treatment (12U/day) of diabetic rats decreased plasma apo AI levels significantly (treated: 32.8 +/- 3.4, untreated: 48.7 +/- 6.2, control: 28.5 +/- 2.4 mg/dl) and normalized plasma apo E levels (treated: 16.1 +/- 1.7, untreated: 5.4 +/- 0.7, control: 15.8 +/- 1.3). Insulin injection (4U/day) to normal rats did not cause any changes in both plasma apo AI and apo E levels. The data indicate that diabetes is not always accompanied by hyperlipidemia, however this inevitably carries apoprotein abnormalities characterized by the high plasma apo AI and low apo E levels, which are reversible with insulin treatment. The changes in the levels of plasma apo AI and apo E could be related to the development of atherosclerosis in diabetes.
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PMID:Reciprocal changes of plasma apo AI and apo E levels in streptozotocin-induced diabetic rats. 644 8

The hyperlipidemias, with hypertension, diabetes mellitus and cigarette smoking, are amongst the major risk factors for the development of atheroma. The inter-relationships of hyperlipidemia and atheroma are complex but both appear to have a strong inherited component. Amongst the multiple genetic factors determining the common forms of hyperlipidemia, the apolipoprotein genes coding for the major peptides of the plasma lipoproteins (chylomicrons, VLDL, LDL and HDL) may be of particular relevance since the latter form a system of inter-converting particles for the delivery of lipid (triglyceride and cholesterol) to peripheral tissues (including the arterial wall). Recently several apolipoprotein genes have been isolated. Particularly interesting results have been obtained with the apolipoprotein AI and CIII genes. The DNA sequence of both genes and their immediate flanking region was determined. The two genes are physically linked and convergently transcribed. The cloning of the apolipoprotein genes made possible a detailed genetic study of patients with defects in lipid metabolism. An altered apo AI gene was shown to be inherited as a Mendelian trait linked to premature atherosclerosis in an affected family. Furthermore, the alteration of the apo AI gene seems to affect the expression of the apo CIII gene. Another DNA polymorphism that generates a new SstI site was shown to be present at low frequency (8%) in a random sample of the population. However, its frequency increased dramatically (42%) in a group of hypertriglyceridemic patients. It is thus not inconceivable that further studies of the genes involved in lipid metabolism will eventually help to replace the present phenotype based classification of lipid metabolism disorders by a genotype based system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein genes and hyperlipidemia. 649 70

A patient with diabetes mellitus is described in whom an unusual xanthomatosis developed involving large areas of the subcutaneous tissue and vocal cords. Few lesions were present on the skin. Plasma lipid, lipoprotein, apolipoprotein, and cholestanol levels revealed normal patterns. Electron microscopy showed macrophages with vacuolar and crystal lipid inclusions. Results of lipid and enzyme analysis of the subcutaneous xanthoma were similar to those of xanthomas derived from a patient with diabetes mellitus and type V hyperlipidemia. The mechanism of this xanthomatosis remains unknown.
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PMID:Normolipemic subcutaneous xanthomatosis. 665 May 39

The relationship between serum lipid, lipoprotein, and apolipoprotein levels and abnormalities of renal function has been investigated in 112 insulin-dependent (type I) diabetic patients. They were subdivided into three matched groups according to the amount of albuminuria: group A (albuminuria less than 20 micrograms/min), group B (albuminuria between 20 and 150 micrograms/min; Albustix negative), and group C (albuminuria greater than 150 micrograms/min; Albustix positive). Twenty-one nondiabetic subjects with albuminuria above 150 micrograms/min but without nephrotic syndrome and/or renal failure and 77 healthy subjects were also studied. Mean total and LDL cholesterol, triglycerides, and apo B were higher, while HDL cholesterol and HDL/LDL cholesterol ratio were lower in group C than in groups A and B; the apo A/apo B ratio was lower in group C than in group A. Differences in apo B and in apo A/apo B ratio were found between groups A and B. No correlation between lipid parameters and amount of albuminuria was observed. Significant differences in lipid concentrations were also found in diabetic patients when compared with nondiabetic subjects with albuminuria and with healthy subjects. The present study confirmed previous reports of lipid disorders in insulin-dependent (type I) diabetes; however, the most important observation was the finding of albuminuria-related differences in lipid parameters in diabetic patients without renal failure. We think that the greater lipid abnormalities observed in diabetic patients with larger amounts of albuminuria might be the consequence both of impairment of glomerular permeability and of the diabetic state.
Diabetes Care
PMID:Lipid abnormalities in insulin-dependent diabetic patients with albuminuria. 673 82

The effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B, and LCAT activity was investigated in 16 hyperlipidemic, non-insulin-dependent diabetes, who were treated for 8 weeks with either placebo or bezafibrate in a double-blind cross-over design. Bezafibrate induced a significant decrease in plasma triglycerides (P less than 0.01), cholesterol (P less than 0.05), VLDL triglycerides (P less than 0.05) and VLDL cholesterol (P less than 0.01), and a significant increase in HDL cholesterol (P less than 0.01), whereas LDL cholesterol remained unchanged. The apolipoprotein AI/apolipoprotein B ratio increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.0001) and the apolipoprotein AI/apolipoprotein AII ratio decreased (P less than 0.0001), indicating an increase in the HDL3 rather than the HDL2 fraction. No significant change in LCAT activity was observed.
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PMID:Effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B and LCAT activity in hyperlipidemic, non-insulin-dependent diabetics. 681 Sep 4

Three probands heterozygous for a mutant of apolipoprotein AI (apo AIMarburg, Utermann et al. 1982a) were detected by screening of 2282 unrelated individuals resulting an a frequency estimate of about 1/750 in the German population. All three probands with apo AIMarburg had hypertriglyceridemia (triglyceride above 250 mg/dl) and subnormal HDL-cholesterol (below 30 mg/dl), but no other lipoprotein abnormalities. The kindreds of two probands with AIMarburg were studied. The family data are consistent with an autosomal codominant inheritance of the trait. A total of 16 heterozygous blood relatives with the mutant AIMarburg were detected in these kindreds. Analysis of the plasma lipid and lipoprotein levels in relation to the apo AI phenotype was complicated by the high prevalence of diabetes mellitus and thyroid disease in one kindred and of hyperlipidemia in both kindreds. No consistent relationship between plasma lipid and lipoprotein levels, and the mutant apo AI could be demonstrated. Instead the mutant apo AI and the dyslipoproteinemia seem to co-exist independently in these kindreds. Three sibs with the homozygous apo E-2/2 phenotype were detected in one kindred, and all three sibs had subnormal LDL-cholesterol and beta-VLDL, e.g., the lipoprotein abnormality characterizing primary dysbetalipoproteinemia. Genetic apo E phenotypes and the apo AI mutant segregated independently, indicating that the structural gene loci for apo E and apo AI are not closely linked.
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PMID:Apolipoprotein AIMarburg: studies on two kindreds with a mutant of human apolipoprotein AI. 681 31

A previous study of low density lipoprotein metabolism by cultured cells focused on the metabolism of normal lipoproteins in vitro by fibroblasts isolated from diabetic patients. No abnormalities were found. We have followed the opposite approach. Using normal human fibroblasts as test cells we compared the metabolism in vitro of low density lipoproteins isolated from diabetic patients before and after metabolic control. We found a significant decrease (p less than 0.02) in internalization and degradation of low density lipoproteins isolated from diabetic patients before metabolic control when compared with those isolated from normal control subjects or from the same patients after metabolic control. The observed changes were mainly apparent in intracellular degradation. To evaluate whether the observed differences in low density lipoprotein behaviour were correlated with lipid or apolipoprotein composition, we measured cholesterol, triglyceride, apolipoprotein B and total protein levels in the low density lipoproteins tested. A significant decrease (p less than 0.05) of the triglyceride/protein ratio was found in post-control low density lipoproteins suggesting that a high triglyceride content may interfere with low density lipoprotein metabolism. The present study represents the first observation that metabolic control in diabetes mellitus can alter low density lipoprotein-cell interaction and suggests a possible mechanism for the enhanced incidence of atherosclerosis in diabetic patients.
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PMID:Surface binding, internalization and degradation by cultured human fibroblasts of low density lipoproteins isolated from type 1 (insulin-dependent) diabetic patients: changes with metabolic control. 704

Based upon a 3-week observation at a summer camp for diabetic children whose medical therapy, metabolic rate, diet, physical exercise and special training could be closely monitored, the following parameters were measured at the beginning and at the end: In whole blood and young erythrocytes HbA1, in serum triglycerides, cholesterol, HDL-cholesterol, as well as apolipoprotein A and B. From these data, the LDL-cholesterol and the atherosclerosis indices (LDL-cholesterol/HDL-cholesterol and apolipoprotein B/apolipoprotein A) were determined. The following results were obtained: the parameters of lipid-metabolism recognized as risk factors for vascular complications such as triglycerides, cholesterol, LDL-cholesterol and apolipoprotein B, were the same as those obtained from a control group of healthy children in the same age. Using HbA1 as the basis for the observations, the risk factors were reduced by normalisation of glucose metabolism. On the other hand, the apolipoprotein A and HDL-cholesterol, well known as protective factors against atherosclerosis, are higher than in the control group and show a further increase with metabolic normalisation. The conclusion is: If medical therapy, metabolic rate, diet, physical exercise and special training are better controlled, the risk of diabetes developing macroangiopathy can be diminished.
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PMID:[Correlations between lipoproteins and glycosylated hemoglobins in juvenile diabetes mellitus (author's transl)]. 709 78

As liquor contains only HDL (High Density Lipoprotein) as a lipoprotein we have studied the changes in the levels of apolipoprotein A, which is the major component of HDL according to the duration of the pregnancy. The study has been carried out in normal and pathological pregnancies. It has been found that the level of apolipoprotein A rises from the 16th week of amenorrhoea of pregnancy to the 26th week and then gradually drops to term. The maximum level is approximately ten times greater than the level of apolipoprotein A at term (a level approximately of 1 mg per litre). This change parallels that of total proteins throughout pregnancy. We have limited our study in pathological pregnancies to the examination of the liquor at the end of pregnancy. The three pathological maternal conditions that have been most frequently found are:--diabetes,--Rhesus-immunisation,--vasculo-renal syndromes. There has been no significant change shown up in the period that we have studied, which was from the 30th to the 38th week of amenorrhoea.
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PMID:[The levels of apolipoprotein A in liquor in normal and pathological pregnancies (author's transl)]. 710 56

Turnover rates of plasma very low density lipoprotein (VLDL) triglyceride (TG) and apolipoprotein-B (apo-B) were significantly increased in age- and weight-matched groups of normolipemic and hyperlipemic mild diabetics, and hyperlipemic moderately severe diabetics when compared with normolipemic controls. As in the normolipemic subjects, a significant correlation between VLDL TG and apo-B turnover rates was found in all diabetic groups, suggesting that integration of TG and apo-B production at synthetic and/or secretory sites is retained in diabetes, thus resulting in increased secretion of VLDL particles of normal composition. In normolipemic mild diabetic subjects, the fractional turnover rates of VLDL TG and apo-B were also significantly increased so that increased removal accompanied increased VLDL production. In the hyperlipemic diabetics, however, the fractional turnover rates were significantly reduced, hence the increased in VLDL removal was not sufficient to compensate for enhanced production. In normolipemic mild diabetic patients, low density lipoprotein (LDL) formation was increased, only a small fraction of VLDL apo-B being removed via a non-LDL pathway, presumably as remnant VLDL. In hyperlipemic mild diabetics, removal of VLDL apo-B via both the LDL and non-LDL pathways was increased. In hyperlipemic moderately severe diabetes, LDL formation was not increased; catabolism of VLDL apo-B through the non-LDL route was however, fivefold greater than normal. We conclude that increased VLDL secretion is a fundamental defect in non-insulin-dependent diabetes. In hyperlipemic individuals, VLDL removal is also impaired. The increase in LDL and/or VLDL remnant formation, regardless of prevailing plasma lipid levels or the severity of diabetes, provides a source of cholesterol which may account for the atherogeneity of this disorder.
Diabetes 1982 Mar
PMID:Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in non-insulin-dependent diabetes mellitus. 715 29


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