Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review is aiming to study the values of apolipoprotein AI and B and plasma lipid levels (total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride) in well-treated diabetic patients, and their possible relationship with hemoglobin A1, body mass index and insulin levels. The study groups were 26 insulin-dependent diabetic (IDDM) patients, 30 non-insulin-dependent diabetic (NIDDM) subjects and 20 non diabetic subjects (controls). Apolipoprotein AI concentrations were similar in the three groups, but apolipoprotein B values and apo B/apo AI ratio were significantly higher in IDDM as related to NIDDM patients (p < 0.001) and to non-diabetic subjects (p < 0.001). We were not able to find significant differences concerning plasma lipid values between the three groups. We found a weak correlation between apo B and hemoglobin AI in IDDM (r = 0.45; 0.02 < p < 0.05), but not in NIDDM patients. Body mass index was not related to the values of apolipoproteins AI and B. We found a positive but weak correlation between insulin levels and triglyceride (r = 0.42), and an inverse one with HDL cholesterol (r = 0.57; 0.02 < p < 0.05) in non-diabetic subjects only, while in NIDDM patients these associations were even less significant. Plasma insulin values strongly correlate to body mass index in both NIDDM (r = 0.64; p < 0.001) and in control subjects (r = 0.73; 0.001 < p < 0.001).
 ...
PMID:Apolipoproteins AI and B and plasma lipid values in well-treated diabetic patients from Romania. 864 98

Cholesterol, triglyceride (TG), and apolipoprotein (apo) B were determined in plasma and in lipoprotein subfractions (VLDL, intermediate-density lipoproteins [IDL], LDL, and HDL) in nonobese NIDDM subjects, who were classified into well-controlled, fairly controlled, or poorly controlled states with or without macrovascular complications (macroangiopathy [MA]). The same analyses were also performed on subjects who had coronary artery disease (CAD) with stable angina pectoris (SA) or unstable angina pectoris (UA) and acute myocardial infarction, cerebrovascular disease (CVD) with atherothrombotic or lacunar infarction, and arteriosclerosis obliterans (ASO). In nonobese NIDDM subjects, the number of apoB-containing lipoproteins (VLDL, IDL, and LDL) increased. This alteration was more prominent in subjects with poorly or fairly controlled disease as well as in subjects with MA, but not in those with well-controlled NIDDM. Cholesterol/apoB in LDL decreased in subjects with poorly or fairly controlled diabetes or with MA and was correlated with low HDL cholesterol. The disorder is characterized by hyperbetalipoproteinemia with elevated LDL cholesterol and small dense LDL. In obese NIDDM subjects, the similar disorder was more pronounced. Glycemic control had less effect and hyperinsulinemia, if present, aggravated the lipid disorder. In those with CAD, the number of IDLs increased and the LDL fraction had the properties of small dense LDL. HDL cholesterol decreased. In those with UA, the LDL number increased without elevation of LDL cholesterol, indicating typical hyperbetalipoproteinemia. The subjects with atherothrombotic brain infarction, an increased number of small-sized LDLs was noted. In those with ASO, the number of VLDL and IDL increased with small LDL. HDL cholesterol decreased in those with CAD, cerebrovascular disease, and ASO. Since similar quantitative and qualitative alterations of apoB-containing lipoprotein have been observed in NIDDM patients as well as in those with macrovascular diseases, diabetic patients are thought to be more susceptible to the initiation and progression of atheromatous lesions in coronary, brain, and peripheral arteries.
 ...
PMID:Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects. 867 86

The review examines the evidence that the supply of cholesterol available for incorporation into nascent lipoprotein particles exerts a regulatory influence on apolipoprotein (apo) B secretion by the liver. Support for this hypothesis comes both from in vitro experiments and from recent observations in normal subjects and patients with dyslipidemia associated with familial hypercholesterolemia, obesity, noninsulin dependent diabetes mellitus, growth hormone deficiency and cholesteryl ester storage disease. The findings do not negate a role for triglyceride synthesis in determining apoB secretion in very low density lipoprotein, but the inhibitory effects on the latter process of pharmacological blockade of cholesterol synthesis or esterification suggest that it is conditional upon an adequate supply of cholesteryl ester.
 ...
PMID:Role of cholesterol in regulating apolipoprotein B secretion by the liver. 872 9

The aim of this study was to verify whether or not the increased prevalence of coronary heart disease (CHD) commonly observed in patients with type 2 diabetes mellitus is related to a genetic background involving restriction fragment length polymorphisms (RFLPs) of apolipoproteins. On the basis of a case-control design, 62 type 2 diabetic patients with CHD (confirmed by clinical history and electrocardiogram) and 62 age- and sex-matched diabetic subjects without CHD were enrolled. In each of them RFLPs of the apolipoprotein CIII gene (S1 or S2 allele) and AI promoter region (A or G allele), together with fasting plasma lipids and apolipoproteins levels, were assessed. The rare S2 allele was found significantly (P = 0.05) more frequently in patients with CHD, and its related S1S2 genotype was associated with higher plasma levels of total cholesterol (P = 0.01), triglycerides (P = 0.007) and apo B (P = 0.001) than the S1S1 genotype. The A allele was more frequent (P = 0.004) in patients without CHD and was associated with lower plasma cholesterol (P = 0.0001), low-density lipoprotein (LDL)-cholesterol (P = 0.0001) and apo B (P = 0.005). The S1/A haplotype was more frequent (P = 0.05) in patients without CHD and was associated with the lowest plasma lipid levels. These results suggest that genetic factors, related to the apo AI-CIII-AIV gene cluster, could play a role in the development of CHD in type 2 diabetic patients, probably through modification of their plasma lipid pattern.
 ...
PMID:Apolipoprotein AI-CIII-AIV genetic polymorphisms and coronary heart disease in type 2 diabetes mellitus. 875 Jul 64

Serum lipoprotein (a) concentrations (Lp(a)) are largely under genetic control, and are strong predictors of coronary heart disease. It has been hypothesised that Lp(a) may contribute to the increased risk of coronary heart disease in familial Type 2 diabetes mellitus. We therefore examined the Lp(a) concentrations and the apolipoprotein (a) (apo(a)) phenotypes in 126 normoglycaemic first degree relatives from families with two or more living Type 2 diabetic patients. These were compared with 147 sex matched normoglycaemic control subjects with no family history of diabetes. Lp(a) concentrations were measured using an enzyme-linked immunosorbent assay (ELISA), and apo(a) isoforms were determined and classified according to the relative mobility of apo(a) on sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), relative to that of apolipoprotein B-100. There were no significant differences in Lp(a) concentrations between the relatives (R) and controls (C): 11.2 (R) vs. 11.1 (C) mg/dl (median). The distribution of apo(a) phenotypes was not significantly different between groups 0.65 (R) vs. 0.67 (C). These results show that first degree relatives at risk of developing Type 2 diabetes do not have abnormal Lp(a) concentrations or apo(a) phenotypes.
 ...
PMID:Lipoprotein (a) concentrations and apolipoprotein (a) phenotypes in normoglycaemic relatives of type 2 diabetic patients. 880 Apr 99

This study examines the activity of two key enzymes of reverse cholesterol transport, cholesterol ester transfer protein (CETP) and lecithin:cholesterol acyl transferase (LCAT) in 21 patients with non-insulin dependent diabetes mellitus (NIDDM) and 21 control subjects. Serum CETP was assessed by measuring plasma-mediated cholesteryl ester transfer between pooled exogenous lipoprotein with endogenous LCAT inhibited--an estimate of CETP mass. CETP activity was determined as cholesteryl ester transfer in the presence of the patients' lipoproteins and LCAT (endogenous assay). LCAT activity was determined in the same assay. There was no significant difference in CETP mass between the diabetic and non-diabetic subjects and there was no correlation between CETP mass and LCAT activity. Using the endogenous lipoprotein assay, CETP was elevated in serum from diabetic patients compared to control subjects (10.05 +/- 1.89 vs. 5.50 +/- 0.53 nmol/ml/h P < 0.05). LCAT was also increased in the diabetic patients (53.63 +/- 4.70 vs. 41.22 +/- 3.40 nmol/ml/h P < 0.05). Serum free cholesterol from diabetic and control subjects correlated with CETP activity measured using endogenous lipoprotein assay (r = 0.77, P < 0.001 and r = 0.82, P < 0.001), and also with LCAT activity (r = 0.76, P < 0.01 and r = 0.79, P < 0.01). There was a negative correlation between CETP activity with the endogenous lipoprotein assay and serum high density lipoprotein (HDL) cholesterol in the diabetic patients (r = -0.38, P < 0.01), but not in control subjects. In a subgroup of 10 control subjects, there was a positive correlation between LCAT activity and apolipoprotein (apo) A-I (r = 0.49, P < 0.05) and apo A-II (r = 0.51, P < 0.05) and also between CETP activity (endogenous assay) and apo A-I (r = 0.87, P = 0.001) and apo A-II (r = 0.63, P < 0.05). No relationship was observed between CETP activity and apo A-I or apo A-II in the diabetic subjects. Thus, serum CETP mass was normal in Type 2 diabetes but CETP activity (endogenous assay) was increased and was related to free cholesterol levels and LCAT activity in both diabetic and non-diabetic subjects.
 ...
PMID:Increased esterification of cholesterol and transfer of cholesteryl ester to apo B-containing lipoproteins in Type 2 diabetes: relationship to serum lipoproteins A-I and A-II. 880 92

We tested the ability of remnant-like particles (RLP) from NIDDM patients to stimulate cholesteryl ester synthesis in human monocyte-derived macrophages. Six NIDDM patients were studied together with 7 non-diabetic subjects. All had apolipoprotein (apo) E3/3 phenotype. RLP were isolated using an immunoaffinity gel mixture of anti apo B-100 and anti apo A-1 monoclonal antibodies coupled to Sepharose 4B. Plasma levels of triglyceride, total cholesterol (chol) and high density lipoprotein-chol were not statistically different, but plasma levels of RLP-chol were significantly (p < 0.05) higher in NIDDM patients (10.5 +/- 2.2 mg/dl) than in non-diabetic controls (5.0 +/- 1.7 mg/dl). The effects of RLP from NIDDM patients on macrophage cholesteryl ester synthesis were estimated. 14C-oleate incorporation into cholesteryl esters in macrophages was significantly (p < 0.01) higher in NIDDM patients with apo E3/3 (0.326 +/- 0.037 nmole/mg cell protein) than in non-diabetic controls with apo E3/3 (0.181 +/- 0.011 nmole/ mg cell protein). It is suggested that RLP from NIDDM play a role in the accumulation of cholesteryl esters and are one of the risk factors for the acceleration of atherosclerosis in NIDDM.
 ...
PMID:Remnant-like particles (RLP) from NIDDM patients with apolipoprotein E3/3 phenotype stimulate cholesteryl ester synthesis in human monocyte-derived macrophages. 889 73

Thirty patients were investigated with hyperlipoproteinaemia, 15 patients with non-insulin dependent diabetes mellitus (NIDDM) and 15 with primary hyperlipoproteinaemia. The patients took 250 mg acipimox (5-metyl-pyrazine-carboxylic acid 4-oxide) 3 times per day for 2 months. Serum examinations were performed before and after 1 and 2 months of acipimox administration. After treatment the cholesterol and triglyceride levels decreased in both groups. Patients with NIDDM had 11% increase of high density lipoprotein-cholesterol (HDL-C) level at the end of the first, and 18% increase at the end of the second month, while patients with primary hyperlipoproteinaemia did not change significantly. The low density lipoprotein (LDL) level did not change significantly in either groups of patients. The apolipoprotein A 1 (apo A 1) levels increased significantly during the second month of acipimox administration. Uric acid levels decreased in both groups, but significant change could be detected mainly in the NIDDM group. Serum glucose level did not change in the non-diabetic patients, while it decreased significantly in the NIDDM group.
 ...
PMID:Treatment possibility of hypercholesterolaemia associated with hypertriglyceridaemia. 940 14

In hypertriglyceridemic states, triglyceride enrichment of high-density lipoprotein (HDL) may play an important role in decreasing the HDL cholesterol and apolipoprotein (apo) A-1 plasma concentration. We have shown previously that HDL particles are transformed into small HDLs when lipolysis is stimulated in vivo or in vitro, and this process is more marked if the HDL is triglyceride-rich. The present study was conducted to determine whether the susceptibility of HDL to transformation can be altered by triglyceride-lowering therapy in humans. Seventeen moderately hypertriglyceridemic individuals (nine with type II diabetes mellitus and eight moderately hypertriglyceridemic nondiabetic subjects) were studied before and after 3 months of triglyceride-lowering therapy with gemfibrozil. Since no significant differences in postprandial and postheparin HDL metabolism were detected between type II diabetic and nondiabetic subjects, results are reported for the two groups combined (N = 17). Fasting HDL was triglyceride-rich with a preponderance of HDL3, and became more enriched with triglycerides postprandially. Heparin administration resulted in a rapid decrease in plasma and HDL triglycerides and an increase in plasma and HDL free fatty acids (FFAs). Postheparin, there was a reduction in HDL size and an increase in the proportion of small (HDL3c) HDL particles (HDL3c constituted 7.1% +/- 1.8% of total HDL preheparin and 26.6% +/- 3.8% postheparin, P < .001). Triglyceride-lowering treatment resulted in a decrease in fasting triglycerides (-54%, P < .001) and HDL triglyceride content (-36%, P = .002), an increase in fasting HDL cholesterol (19%, P = .004), and proportionately fewer (13.2% +/- 2.1%, P < .001) HDL3c particles formed postheparin. Postheparin HDL size correlated inversely with the fasting triglyceride level (r = -.55, P < .001) and HDL triglyceride concentration (r = -.34, P = .02). These results show that the postprandial increase in triglyceride levels in hypertriglyceridemic subjects is associated with increased production of small HDL particles when lipolysis is stimulated, and that lipid-lowering therapy can contribute to favorably reduce this postprandial production of small HDL particles. Further studies are needed to clarify how these abnormalities ultimately lead to a decrease of plasma HDL cholesterol and apo A-1 in hypertriglyceridemic states.
 ...
PMID:Production of small high-density lipoprotein particles after stimulation of in vivo lipolysis in hypertriglyceridemic individuals: studies before and after triglyceride-lowering therapy. 947 77

Non-insulin dependent diabetes (NIDDM) is associated with an increased risk of peripheral vascular disease (PVD), but within the diabetic population the relationship between lipid profile and PVD has not been clearly defined. In this study we examined the association of lipid parameters and in particular low density lipoprotein (LDL) particle size, with the presence of PVD in subjects with and without NIDDM. 41 NIDDM patients and 31 non-diabetic subjects with PVD in the absence of rest pain or ulceration, defined by ankle-brachial index measurements and duplex scanning, were compared with 41 NIDDM and 31 euglycemic control subjects of comparable age and sex, without PVD. In both groups those with PVD were found to have significantly elevated triglycerides (2.7 [2.2-3.3] versus 1.9 [1.6-2.2] mmol/l; P < 0.05 in the diabetic group and 2.0 [1.6-2.3] versus 1.4 [1.1-1.5] mmol/l; P < 0.05 in the non-diabetic group), decreased apolipoprotein A1 (124 +/- 3 versus 139 +/- 5 mg/dl; P < 0.01 in the diabetic group and 133 +/- 4 versus 147 +/- 4 mg/dl; P < 0.05 in the non-diabetic group) and decreased LDL particle size (25.4 +/- 0.1 versus 25.8 +/- 0.1 nm; P < 0.01 in the diabetic group and 26.0 +/- 0.1 versus 26.3 +/- 0.1 nm; P < 0.05 in the non diabetic group). In the non-diabetic group apolipoprotein[a] (365 [239-554] versus 184 [17-266] U/l; P < 0.01), total cholesterol (6.3 +/- 0.2 versus 5.6 +/- 0.2 mmol/l; P < 0.05), LDL cholesterol (4.1 +/- 0.2 versus 3.6 +/- 0.2 mmol/l; P < 0.05) and apolipoprotein B (146 +/- 8 versus 117 +/- 5 mg/dl; P < 0.05) were also found to be associated with PVD although these associations were not observed in the group with diabetes. In addition, 11 NIDDM subjects and 11 non-diabetic subjects with rest pain or ulceration were compared to the corresponding groups with uncomplicated PVD and had lipid profiles with significantly lower levels of total cholesterol and LDL cholesterol. We conclude that the dyslipidemic profile characterized by increased triglyceride level, decreased apolipoprotein A1 level and small dense LDL is associated with uncomplicated PVD in both NIDDM and non-diabetic subjects.
 ...
PMID:Lipid levels and peripheral vascular disease in diabetic and non-diabetic subjects. 954 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>