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)

Non-insulin-dependent diabetes mellitus (NIDDM) is associated with increased very-low-density lipoprotein (VLDL) and triglyceride concentrations as abnormalities of low-density lipoprotein (LDL) composition. Because fish oil has a strong triglyceride lowering effect in case of normolipemic subjects, we investigated the influence of supplementary fish oil diet in patients suffering from NIDDM (n = 19), who until now were not treated by drugs but only by diet. The study was started with a placebo-run-in-period for four weeks (phase I, 6 g rape seed oil capsules/d), followed by a verum period for twelve weeks (phase II, 6 g fish oil concentrate capsules/d), and a wash-out-period for four weeks (phase III, 6 g rape seed oil capsules/d). The fish oil supplementation contained at least 3 g eicosapentenoic and docosahexenoic acid. The lipoproteins, apolipoproteins, blood glucose, and insulin level (fasting and after load test) were checked at the beginning and at the end of each phase. In comparison to the placebo rape seed oil supplementation, the fish oil diet effected a decrease of serum triglycerides by 29%. LDL-cholesterol increased by 9%, HDL-cholesterol by 9% (especially HDL2-cholesterol), and apolipoprotein B by 4%. Apolipoprotein A-I was reduced by 9%. The fasting blood glucose and the glucose load test as the insulin level (fasting and after load test) showed no significant changes at the end of the verum period in comparison to the run-in-phase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of fish oil concentrate on the lipoprotein profile of patients with type II diabetes mellitus]. 154 65

Serum concentrations of apolipoproteins A-I, A-II, B, C-I, C-II, C-III and E were determined by electroimmunoassay in 56 patients with chronic renal failure (CRF) in the predialytic phase. The results were compared with those obtained in asymptomatic normolipidemic subjects, patients with type IV hyperlipoproteinemia, and patients with type II diabetes mellitus. CRF patients had reduced concentrations of ApoA-I and ApoA-II, normal levels of ApoB and ApoC-I, and increased concentrations of ApoC-II and, in particular, of ApoC-III. There was a significant reduction in the levels of ApoE, especially in male patients. In comparison with type IV, hyperlipoproteinemic patients, CRF patients had lower concentrations of ApoA-I, ApoA-II, ApoB, ApoC-I and, particularly, ApoE; there was no difference in ApoC-III levels reflecting the hypertriglyceridemia common to both disorders. Similar but less marked differences were also found in comparison with type II diabetics. The findings suggest that in CRF, the accumulation of ApoC-III-enriched lipoprotein particles accompanied by a moderate hypertriglyceridemia may be caused more probably by an impaired catabolism than overproduction of triglyceride-rich lipoproteins. CRF patients with vascular disease tended to have higher serum concentrations of triglycerides, cholesterol and ApoB and lower ApoA-I/ApoC-III and ApoA-I/ApoB ratios than patients without vascular disease.
 ...
PMID:Serum apolipoprotein profile of patients with chronic renal failure. 366 95

Elevated levels of plasma triglycerides (TG) and reduced concentrations of HDL cholesterol are very common in patients with diabetes, particularly NIDDM. Although regulation of the plasma concentrations of VLDL, the major TG-rich lipoprotein is extremely complex, it is clear from in vivo kinetic studies that increased rates of secretion of VLDL into plasma is almost uniformly present in patients with NIDDM and hypertriglyceridemia. Recent studies at the cellular level indicate that increased fatty acid flux to the liver, also common in NIDDM (and other insulin-resistant states associated with elevated plasma TG levels), will stimulate the assembly and secretion of apoprotein (apo) B-containing lipoproteins by targeting apoB for secretion rather than intracellular degradation. Increased rates of secretion of VLDL into plasma appears to drive the exchange of TG from these lipoproteins for HDL cholesteryl ester. This exchange, which occurs in plasma, is facilitated by cholesteryl ester transfer protein, and generates a TG-enriched HDL that is a substrate for either hepatic lipase or lipoprotein lipase. When the TG in HDL is hydrolyzed, the resultant particle is smaller, and this appears to affect the binding of the major HDL protein, apoA-I. ApoA-I dissociates from the smaller, lipid-poor HDL, and the free apoA-I (molecular weight 28,000) can be filtered by the glomerulus in the kidney and most likely is degraded in renal tubular cells after reabsorption. Thus, increased free fatty acid transport in plasma, a common abnormality in insulin-resistant states, may be the underlying driving force for the two common lipid abnormalities seen in diabetes.
 ...
PMID:Diabetic dyslipidemia: basic mechanisms underlying the common hypertriglyceridemia and low HDL cholesterol levels. 867 85

The presence or absence of coronary artery disease (CAD) in diabetic patients has been related to the level of circulating plasma lipoproteins. This study examines whether there is a relationship between the actual severity of CAD and the plasma concentration of major classes of plasma lipoproteins (HDL, LDL, triglyceride-rich lipoproteins (TRL), and their Sf 12 to 60 and Sf 60 to 400 subfractions), particularly the numbers of lipoprotein particles, in men and women with type 2 diabetes. 174 diabetic patients (136 men, 38 women) who underwent angiography were studied. Nine specific coronary segments were scored. The population was divided into tertiles according to the angiographic severity of their coronary disease: mild CAD: coronary score 1 to 10; moderate CAD: coronary score 11 to 13; or severe CAD: coronary score 14 to 22. The main findings were that the numbers of particles (as reflected by the apoB levels) of the TRL were greater in those with moderate and severe disease than in those with mild disease (P = .001). There was a significant correlation between the coronary score and the apoB in TRL (P = .006). There were parallel but nonsignificant changes in triglyceride levels. ApoA-I was lower in patients with moderate and severe disease (P = .01). These differences were more striking in women than they were in men. There were no differences in plasma, LDL, or HDL cholesterol or in LDL apoB or Lp(a). Multiple linear regression analysis, when adjusted for sex, age, and BMI, showed that three lipid variables (TRL apoB, LDL cholesterol, and plasma apoA-I) significantly and independently predicted the coronary score. This study demonstrates that in type 2 diabetes, the severity of angiographically evaluated CAD is positively related to the numbers of TRL particles in the plasma. This relationship is stronger in women than in men, and it is independent of HDL and LDL.
 ...
PMID:The severity of coronary atherosclerosis in type 2 diabetes mellitus is related to the number of circulating triglyceride-rich lipoprotein particles. 943 15

Non-insulin-dependent diabetes mellitus (NIDDM) is associated with low high density lipoprotein (HDL) cholesterol and apoA-I, related to an increased apoA-I fractional catabolic rate. This stable isotope kinetic experiment, using L-[1-(13)C] leucine, was designed to study the effect of insulin therapy on HDL apoA-I and A-II metabolism in poorly controlled NIDDM patients. A kinetic study was performed in five control subjects and in six NIDDM patients before and two months after the introduction of insulin therapy. ApoA-I and A-II were modelled using a monoexponential function. Insulin treatment was able to correct neither the low HDL apoA-I concentration observed in NIDDM patients (1.14+/-0.19 vs. 1.16+/-0. 12 g l(-1) (controls: 1.33+/-0.14)), nor the HDL apoA-I hypercatabolism (0.39+/-0.11 vs. 0.34+/-0.05 pool d(-1), (controls: 0.23+/-0.01, P< 0.01)). HDL apoA-I production rate was increased in NIDDM patients compared to control subjects and was not modified by insulin (0.45+/-0.12 vs. 0.39+/-0.08 g d(-1) l(-1), (controls: 0. 31+/-0.04, P< 0.05)). HDL apoA-II kinetic parameters were initially not significantly different between NIDDM patients and control subjects, and were not modified by insulin. The decreased insulin sensitivity, assessed by the insulin suppressive test, was not modified by insulin therapy in NIDDM patients. HDL apoA-I fractional catabolic rate was significantly correlated to HDL triglyceride/cholesteryl ester and triglyceride/protein ratios, which were significantly higher in NIDDM patients than in controls and were not modified by insulin therapy. The persistence of insulin resistance and of high neutral lipid exchanges between triglyceride rich lipoproteins and HDL in insulin-treated NIDDM patients probably explain the inefficiency of insulin therapy to correct HDL apoA-I metabolic abnormalities.
 ...
PMID:Inefficiency of insulin therapy to correct apolipoprotein A-I metabolic abnormalities in non-insulin-dependent diabetes mellitus. 1099 59

Lipoprotein (a) is a new independent coronary risk factor, but the role of lipoprotein (a) in type 2 diabetes remains controversial. The objective of this study was to demonstrate the relationship between the level of lipoprotein (a) and the coronary artery diseases (CAD) in type 2 diabetes. Recruitment was carried out in 3 groups of patients: Group 1: 110 control subjects, Group 2: 115 diabetics (D), Group 3: 105 diabetics with CAD (DC). The mean age was, 51 + 7; 52 + 6; 56 + 6 respectively. Total cholesterol, triglyceride, HDL-C, LDL-C, Apo A-I, Apo B and lipoprotein (a) were measured for the patients. The Lp (a) level was significantly higher in the diabetic groups as compared to the controls (p < 0.05), but this level was different between D and DC: 312 + 232 vs 347.8 + (NS). However, when the Lp (a) level is higher than 300 mg/ml, there is a significant difference between DC and D (53% vs 42% p = 0.05). There is no correlation between Lp level and total cholesterol; however, there is a significant variation of Lp (a) level with LDL-C (r = -0.14, P = 0.01). There is a negative correlation between Lp (a) and HDL-C (r = -0.13, p = 0.03), Lp (a) and ApoA-I (r = - 0.11, p = 0.05); but there is a positive correlation between Lp (a) and ApoB (r = 0.14, p = 0.02). Lp(a) level higher than 300 mg/L constitutes a coronary risk factor in type 2 diabetes. This contributes, with the other lipid disorders, to the increase of the coronary risk factors in diabetes.
 ...
PMID:[Lipoprotein (a) and ischemic heart diseases in patients with type 2 diabetes]. 1507 42

The ATP-binding cassette transporter 1 (ABCA1) is a trans-membrane peptide that is involved in the lipidification of ApoA-I. ABCA1 gene was initially implicated in Tangier disease and familial hypoalphalipoproteinemia and has been shown to be associated with coronary artery disease and atherosclerosis as well. Recently, a haplotype in ABCA1 gene was associated with increased risk of type II diabetes mellitus (DM). In this report, a relationship between ApoA-I, DM and ABCA1 has been emphasized.
 ...
PMID:ABCA1, ApoA-I and type II DM. 1600 32

The lipid triad is the association of small, dense (sd) low-density lipoprotein (LDL), low high-density lipoprotein (HDL), and hypertriglyceridemia, all of which play a role in coronary artery disease in patients with type 2 diabetes. Although statins have demonstrated clear positive effects on cardiovascular morbidity/mortality in patients with diabetes and on single components of the lipid triad, it remains controversial whether they affect all components of the triad in these patients. Therefore, we performed a single-center, parallel-group, prospective, randomized, open-label, blinded-endpoint (PROBE)-type comparison of fluvastatin extended-release (XL) 80 mg (n=48) and simvastatin 20 mg (n=46), each given once daily for 2 months to patients with type 2 diabetes with the lipid triad, who were enrolled after a 1-month lifestyle modification and dietary intervention program. After fluvastatin therapy, LDL (-51%; P<.01), apolipoprotein B (ApoB; -33%; P<.01), intermediate-density LDL (idLDL) (-14.3%; P<.05), sdLDL (-45%; P<.01), and triglycerides (-38%; P<.01) were significantly decreased, and HDL (+14.3%; P<.05) and apolipoprotein A-I (ApoA-I; +7%; P<.05) were increased; large buoyant (lb) LDL did not change (P=NS). Simvastatin therapy decreased LDL (-55.1%; P<.01), ApoB (-46%; P<.01), lbLDL (-33.3%; P<.05), idLDL (-22.7%; P<.05), sdLDL (-33.3%; P<.05), and triglycerides (-47.9%; P<.01); HDL was not changed (P=NS) after simvastatin, but ApoA-I was increased (+11.3%; P<.01). HDL increases (P<.01) and sdLDL decreases (P<.01) were significantly greater after fluvastatin compared with simvastatin therapy; LDL, triglycerides, ApoB, and idLDL changes were similar after both therapies (P=NS), and lbLDL decreases were greater with simvastatin therapy (P<.05). With both treatments, classic mean LDL and ApoB target levels were achieved in most patients. We conclude that the lipid triad can be controlled with fluvastatin XL 80 mg in patients with type 2 diabetes.
 ...
PMID:Effects of fluvastatin slow-release (XL 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes. 1651 Mar 70

The present study investigated genetic variation in the 3' flanking region of ApoA-I (PstI), the 3' untranslated region of ApoC-III (SstI) and intron 2 of ApoA-IV (XbaI) in 435 type 2 diabetes mellitus patients, divided according to the presence or absence of coronary heart disease (CHD). Uncommon allele frequencies (P2, S2, X2) were 17.5%, 32.5%, 16.2% and 29.5%, 17.9%, 13.8% in patients with and without CHD, respectively. Linkage disequilibrium (D' = 0.31-0.73, p<0.01) was observed in all diallelic pairs except XbaI/PstI and XbaI/SstI in patients having CHD. Haplotype analysis revealed that P1-S2-X1 is a susceptibility haplotype that increases the risk of CHD in diabetes (OR 2.85, CI 1.51-5.61), exacerbating risk (OR 3.57, CI 1.81-7.45) even after adjustment for confounders. The findings in the present study suggest that each unit of P1-S2-X1 in diabetes increases the risk of CHD by a factor of 1.37+/-0.307 (beta + SE), which is manifest in its multiplicative mode.
 ...
PMID:The ApoAI-CIII-AIV gene cluster and its relation to lipid levels in type 2 diabetes mellitus and coronary heart disease: determination of a novel susceptible haplotype. 1765 46

In order to test whether hyperlipidaemia and glycaemic control can be improved among diabetes patients by dietary supplementation with purified omega-3 fatty acids, we carried out a double-blind, placebo-controlled trial on 50 type 2 diabetes patients randomized to 2 g/day purified omega-3 fatty acids or placebo for 10 weeks. Fasting triglycerides decreased significantly with supplementation relative to placebo (P = 0.01). There was a significant decrease in ApoB-100 and malondialdehyde compared to baseline values and compared to the control group. Omega-3 fatty acids had no significant effect on serum lipid levels, ApoA-I, glucose, insulin and HbA1c.
 ...
PMID:Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients. 1856 22


1 2 3 Next >>