Disease relevance of Tgl1

• We hypothesize that the following pathogenic pathway might occur in the course of type 2 diabetes: increased apoA-II level causes a rise in plasma triglyceride level and glucose intolerance, resulting in hyperglycemia, which in turn might further increase apoA-II gene transcription [1].
• The diabetic nontransgenic mice developed hypercholesterolemia (plasma total cholesterol level: 4.55 +/- 1.32 vs. 1.97 +/- 0.13 mmol/l [176 +/- 51 vs. 76 +/- 5 mg/dl]) and hypertriglyceridemia (plasma triglyceride level: 0.82 +/- 0.29 vx. 0.42 +/- 0.11 mmol/l [73 +/- 26 vs. 37 +/- 10 mg/dl]) compared with values before induction of diabetes [2].

High impact information on Tgl1

• Total absence of the insulin receptor (IR), demonstrated in the homozygous mutant mice, also resulted in other metabolic disorders: plasma triglyceride level could increase 6-fold and hepatic glycogen content could be five times less as compared with normal littermates [3].
• Overexpression of Rad in muscle worsens diet-induced insulin resistance and glucose intolerance and lowers plasma triglyceride level [4].
• Taking lower tendency of triglyceride level of RIP-G Tg into consideration, these results may indicate that the suppression of insulin secretion is likely due to the effect of desacyl ghrelin on insulin sensitivity [5].
• Ethanol drinking did not cause any appreciable change in plasma triglyceride level and metabolism of adipose tissue [6].
• Partial recovery was indicated by a decrease in the hepatic triglyceride level of 16 mg. per gm. by 14 weeks of exposure to 1000 p.p.m. Electron microscopic evaluation revealed that cytoplasmic altertions were most severe in centrilobular hepatocytes in the 1000 p.p.m. group and were mild to minimal in the 250 p.p.m. group [7].

Associations of Tgl1 with chemical compounds

• Furthermore, in animals, these 6alpha-hydroxylated bile acid analogs exhibit a unique pharmacokinetic profile and do not increase the serum triglyceride level; therefore, they may represent a novel class of therapeutic agents for cholesterol management [8].
• Hepatic triglyceride level was also decreased (by 100%, P<0.001) by co-treatment with fenofibrate [9].
• A separate experiment with mice on chow diet confirmed the aberrant steatotic effect of ethanol in C3-/-mice: 4 hours after acute dosing of ethanol the liver triglyceride level had increased by 138% in C3+/+ mice (P<0.001), but only by 64% in C3-/- mice (n.s.). CONCLUSION [10].
• Triglyceride level in heart and liver was dose-dependently reduced by histidine or carnosine treatments (P < 0.05); however, only 1 g/l histidine and carnosine treatments significantly reduced cholesterol level in heart and liver (P < 0.05) [11].
• Some of these compounds were evaluated for their glucose lowering capability and their effects on the triglyceride level in alloxan diabetic mice [12].

Regulatory relationships of Tgl1

• Reduced mitochondrial and peroxisomal fatty acid oxidation may explain the increased hepatic triglyceride level induced by TNFalpha [13].

Other interactions of Tgl1

• OBJECTIVE: ApoAV, a newly discovered apoprotein, affects plasma triglyceride level [14].
• In aurothioglucose-induced obese mouse, 1 suppressed the body and liver weight increase, significantly ameliorated the triglyceride level in the liver, and also reduced the deposition of uterine fat-pads [15].
• Plasma cholesterol and triglyceride level of group A was strikingly lower than that of group B. No difference was found in the lipid composition of beta-VLDLs between both groups [16].

Analytical, diagnostic and therapeutic context of Tgl1

• Globin digest (GD), prepared from globin by acidic protease treatment, suppressed the elevation of serum triglyceride level in not only total but also chylomicron fraction after oral administration of olive oil [17].
• The plasma and hepatic triglyceride level was only lowered by the lovastatin supplement, while the hepatic cholesterol content was lowered by both the naringin and lovastatin supplements compared to the control group [18].

References