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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of insulin on the lipid values of nonobese non-insulin-dependent diabetic (NIDDM) Arab women requiring insulin was investigated to find whether these patients have the same coronary artery risk factor related to lipid levels. In this study, 55 NIDDM women on insulin therapy (mean age 28 +/- 8.1 yr and duration of disease 5 +/- 1.2 yr) and 70 control subjects (matched for sex, age, and body mass index) were studied for their plasma levels of lipids, lipoproteins, and apolipoproteins. Concentrations of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride (TG), LDL TG, high-density lipoprotein triglyceride (HDL TG), phospholipid, glucose, glycosylated hemoglobin (HbAtc), apolipoprotein B (apoB), LDL-apoB, and apoB/apoAl were significantly elevated in diabetic women compared with control subjects. There was no significant change in the levels of apoAll in plasma and lipoprotein fractions. Concentrations of HDL cholesterol (chol), HDL2-chol, HDL3-chol, plasma apoAl, HDL2-apoAl, HDL3-apoAl, and HDL-apoAl were significantly lower in diabetic women than in control subjects. There was no significant correlation between glucose or HbAtc and most of the lipids, lipoprotein lipids, and apolipoproteins measured. Despite normal body weight and insulin therapy, abnormalities in lipids, lipoprotein lipids, and apoB persisted in NIDDM patients compared with control subjects. Our data may favor an enhanced affinity toward atherosclerosis in these patients.
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PMID:Lipoproteins and apolipoproteins in young nonobese Arab women with NIDDM treated with insulin. 265 41

The aim of the present work was to determine and analyse the nutritional status and plasma lipid levels in diabetic and control subjects dependent on the type of lipidemia. The investigations involved four groups: controls with normal lipidemia, diabetic (NIDDM) subjects with normal lipidemia, persons with hyperlipidemia type IV, and without diabetes mellitus, and diabetic subjects with hyperlipidemia type IV. The values for the concentrations of plasma triacylglycerol, cholesterol, phospholipids and HDL-phospholipids were significantly higher in both diabetic groups than in controls. The values for the relative amount and concentration of HDL-cholesterol were significantly lower in diabetics than in the control groups.
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PMID:Nutritional status and plasma lipids in diabetic subjects. 274 21

The present study assesses the impact of variations in the amount of fiber in high carbohydrate diets on carbohydrate and lipid metabolism in NIDDM. The amount and source of carbohydrate, and source of dietary fiber, were held constant. Two 4-wk diet periods were randomly assigned and all subjects completed both dietary periods. Diets were identical in the proportion of carbohydrate, fat, protein, P/S ratio, and cholesterol. The normal fiber diet contained 11 g/1000 kcal, while the high fiber diet contained 27 g/1000 kcal. The results showed no significant difference in fasting plasma glucose and insulin, day-long glucose and insulin, fasting hemoglobin AIc, or 24 h urinary glucose. Fasting plasma triglyceride and VLDL-triglyceride, as well as fasting plasma cholesterol, LDL-cholesterol, and HDL-cholesterol were also unchanged. In conclusion, an increase in the fiber content from 11 to 27 g/1000 kcal did not lead to measurable improvements in overall plasma glucose, insulin, or lipid metabolism.
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PMID:To what extent does increased dietary fiber improve glucose and lipid metabolism in patients with noninsulin-dependent diabetes mellitus (NIDDM)? 300 63

The addition of vegetable fibres to the diabetic diet has been reported to ameliorate glycaemic and plasma lipid profiles, and Guar flour seems to obtain the best results. At its usual dose, Guar produces several gastro-intestinal side effects. A lower dose (4 + 4 g/day) was therefore employed in 10 non-insulin dependent diabetics (NIDD). The following parameters were measured at the end of treatment and after a control period: HbA1 levels, hepatic glucose production (3H-Glucose infusion), peripheral sensitivity to insulin and insulin secretion (hyperglycaemic clamp), and specific insulin binding to isolated monocytes. The ultracentrifugal plasma lipid pattern was also measured. No significant body weight change was recorded during the study. A significant glycaemic and insulinaemic decrease in the fasting state was observed after Guar, together with a significant decrease of HbA1 levels (from 8.5 +/- 0.4 to 7.9 +/- 0.4%, p less than 0.05) and amelioration of peripheral sensitivity to insulin (M/I = 14.3 +/- 6.6 versus 24.3 +/- 8.8, p less than 0.025; 50% increase of insulin binding to circulating monocytes) without significant variation of the fasting hepatic glucose production. Decreased B-cell stimulation by flattening post-prandial glycaemic peaks may be an explanation of the reduction of insulin resistance via down-regulation mechanism. As far as the lipid profile is concerned, a significant reduction in total and LDL cholesterol (p less than 0.05 and p less than 0.01) and an increase in HDL-phospholipids (p less than 0.05) were recorded after Guar. These results suggest that Guar in low doses is well accepted and can contribute to a better glycaemic and lipaemic control in NIDDM.
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PMID:Moderate guar-gum addition to usual diet improves peripheral sensitivity to insulin and lipaemic profile in NIDDM. 300 79

In diabetes, altered lipoprotein metabolism is one of the factors which accelerates the process of atherogenesis. In NIDDM, plasma triglyceride levels are increased and HDL levels are, independently, decreased. In order to increase HDL levels, good metabolic control and prolonged, near perfect, control of lipoprotein metabolism are required. In NIDDM, there is a direct relationship between lipoprotein lipase activity and HDL levels. Optimal insulin therapy gives improved diabetic control, and in the long term will improve the lipoprotein profile in these diabetics. Factors affecting lipid metabolism are discussed, and the importance of improving the lipoprotein profile in diabetics is emphasized.
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PMID:Atherogenic factors in diabetes: the role of lipoprotein metabolism. 307 93

In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins. We studied the glycation of HDL of patients with either type 1 or type 2 diabetes compared with that of control subjects. Although a basal glycation was detectable in HDL of normal individuals, this increased by about 400% in HDL of both groups of diabetic patients. The degree of HDL glycation was positively correlated with blood glucose concentration. All the HDL apoproteins were glycated but the glycation of apo A-I represented about 80% of the total HDL. These data were compared to those obtained in vitro after incubation of normal apo A-I either as free molecular species or as phospholipid/apo A-I complex, in the presence of glucose (0 to 80 mmol/l) at 37 degrees C. The resulting apo A-I glycation was dependent upon both time of incubation and glucose concentration and was largely increased in the presence of phospholipids. These data suggest that the in vivo glycation of HDL apoproteins might depend upon glucose concentration but might also be partly influenced by their lipid environment.
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PMID:Characterization of the non enzymatic glycation of high density lipoprotein in diabetic patients. 313 9

Coronary heart disease in insulin-dependent (IDDM) and in non-insulin-dependent diabetes (NIDDM) is associated with lipid and lipoprotein changes favouring atherosclerosis. Whether lipid and lipoprotein abnormalities are associated also with peripheral vascular disease in both types of diabetes is largely unknown. Therefore, we studied lipid and lipoprotein levels and their association with claudication in a representative sample of diabetic and non-diabetic subjects in East Finland. Altogether 87 subjects had IDDM (43 men, 44 women), 264 subjects NIDDM (126 men, 138 women) and 120 subjects were non-diabetic controls (63 men, 57 women). Patients with IDDM had an increased level of HDL and HDL2-cholesterol and patients with NIDDM a decreased level of HDL and HDL2-cholesterol and an increased level of total, LDL and VLDL triglycerides than did non-diabetic subjects. Analyses in both types of diabetes by claudication status revealed that total and LDL-cholesterol and total and VLDL triglycerides tended to be higher and HDL and HDL2-cholesterol lower in those having claudication as compared to those without a claudication symptom. Similarly, total cholesterol/HDL-cholesterol ratio and LDL-cholesterol/HDL-cholesterol ratio were also more atherogenic in patients with claudication than in those without claudication. In conclusion, our results indicate that in both types of diabetes peripheral vascular disease is associated with lipid and lipoprotein abnormalities favouring atherosclerosis.
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PMID:Lipid and lipoprotein abnormalities in diabetic patients with peripheral vascular disease. 321 81

Based on the data reviewed, it is necessary to conclude that diabetes is associated with profound changes in HDL metabolism. However, once we go beyond this simple generalization, it is apparent that the relationship between diabetes and HDL metabolism is not a simple one. A good deal of the complication evolves from the fact that IDDM and NIDDM seem to affect HDL metabolism quite differently, with the only apparent similarity the fact that plasma HDL-cholesterol concentration can be low in untreated patients with either IDDM or NIDDM. Thus, in patients with IDDM the primary event seems to be related to the insulin-deficient state, which results in a decrease in HDL turnover rate and resultant decline in plasma HDL-cholesterol concentration. In contrast, HDL turnover appears to be accelerated, not reduced in patients with NIDDM, and the low plasma HDL-cholesterol concentration is a consequence of the increased turnover rate. In addition, patients with NIDDM are not absolutely insulin deficient, and available evidence suggests that the higher the plasma insulin level, the lower the plasma HDL-cholesterol concentration in these patients. The differences noted above in the effect of IDDM and NIDDM on HDL metabolism are of great interest, and, unfortunately, not very well understood. There is, however, one additional difference, which may be of paramount clinical importance. For reasons not totally clear, plasma HDL-cholesterol concentrations in patients with IDDM treated with insulin are not lower than normal, and even tend to be higher than these values in a nondiabetic population. Possibly as a result of this phenomenon, there is no evidence that changes in plasma HDL-cholesterol concentration play a role in the development of macrovascular complications in IDDM. Although it is apparent from the considerations discussed in this review that a great deal more needs to be learned about the effect of insulin deficiency on HDL metabolism, changes in HDL metabolism do not appear to be clinically important in patients with IDDM. Unfortunately, this does not appear to be the situation in patients with NIDDM. Plasma HDL-cholesterol concentrations are lower than normal in patients with NIDDM, and this finding seems to be related to increased morbidity and mortality from CAD. Furthermore, there is no form of anti-diabetic treatment, irrespective of how effective it has been in achieving glycemic control, that has been shown to substantially increase plasma HDL-cholesterol level. Indeed, it has been difficult to demonstrate a consistent effect of any therapeutic approach on plasma HDL-cholesterol concentration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:HDL metabolism in diabetes. 330 Dec 37

The glucagon-C-peptide test was evaluated as a predictor of the requirement of insulin therapy in type 2 diabetes mellitus. Endogenous insulin secretory capacity was measured in a population of 150 insulin-treated adult diabetic patients by determining postprandial glucagon-stimulated plasma C-peptide concentration (Novo, antiserum M 1230). Eleven subjects with C-peptide levels above 1.0 nmol/l comprised the subgroup in which the previously started insulin therapy was discontinued. After an observation period of a week in hospital the metabolic control of the patients was followed in an outpatient clinic for twelve months. During the observation period one patient was managed on diet alone, eight subjects required oral hypoglycaemics agents and two required the reinstitution of insulin therapy. Mean fasting blood glucose and GHbA1 (glycosylated haemoglobin) of non-insulin dependent diabetics increased during the observation period (from 8.8 to 11.8 mmol/l, p less than 0.001, and from 12.2 to 14.1%, p less than 0.05, respectively). No significant changes were found in total or HDL-cholesterol or triglyceride levels. The findings demonstrate that the glucagon-C-peptide test can be used as an aid in judging whether the withdrawal of insulin may be considered without excessive risk of developing diabetic ketoacidosis. However, the test cannot be used as the only criterion when assessing the need for exogenous insulin in type 2 diabetes. Meticulous monitoring of blood glucose levels is necessary when insulin therapy is withdrawn, because diabetic patients with peripheral insulin resistance may not maintain satisfactory glycaemic control without exogenous insulin despite of high residual endogenous insulin secretion.
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PMID:Glucagon-C-peptide test as a measure of insulin requirement in type 2 diabetes: evaluation of stopping insulin therapy in eleven patients. 331 47

Thirty patients with NIDDM and severe hyperglycemia (fasting plasma glucose greater than 200 mg/dl) were initiated on insulin therapy. Lipoprotein concentrations were measured by the Vertical Autoprofile procedure before insulin therapy and 1, 3, 6 and 26 weeks after insulin initiation. Patients were divided into 4 phenotypes based on their pretreatment lipoprotein profile: HyperVLDL (elevated VLDL), HyperLDL (elevated LDL), HyperVLDL-LDL (elevated VLDL and LDL), and non-hyperlipidemic. There were no differences in the initial fasting plasma glucose, Hgb Alc, or fasting free insulin concentrations between the groups. Both the HyperVLDL and HyperLDL groups had significantly lower HDL-C concentrations that the non-hyperlipidemic group and the HyperVLDL-LDL group had significantly higher IDL-C than any of the other groups. Insulin therapy resulted in similar decreases in fasting plasma glucose and increases in fasting free insulin concentrations in all 4 groups. HDL-C increased in all 4 groups. The most marked improvements in HDL-C were seen in the non-hyperlipidemic (+37%) and HyperLDL (+42%) groups while the HyperVLDL group had only an 18% increase. VLDL-C fell in all groups but in the HyperVLDL group it fell dramatically to almost normal levels within the first week, whereas it took 6 weeks for the HyperVLDL-LDL group to reach its VLDL-C nadir and this was still significantly higher than normal. LDL-C improved modestly in only the HyperLDL patients after 6 weeks of insulin therapy. There were no statistically significant changes in either the IDL-C or Lp(a)-C in any of the groups during insulin therapy. The changes in HDL-C and IDL-C were negatively correlated with the fasting plasma glucose and Hgb Alc but not with the free insulin concentration. We conclude that: 1) Insulin therapy can cause dramatic improvements in HDL-C and VLDL-C while it has only a mild suppressive effect on LDL-C and no statistically significant effect on IDL-C or Lp(a)-C. The degree of improvement in the lipid profiles varied considerably between the different lipid phenotypes. 2) The hyperlipidemic phenotypes seen in these patients appear to be determined primarily by factors other than the degree of hyperglycemia and hypoinsulinemia.
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PMID:Effect of insulin therapy on lipoproteins in non-insulin dependent diabetes mellitus (NIDDM). 331 86


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