Increased fat absorption and impaired fat clearance cause postprandial hypertriglyceridemia in Spontaneously Diabetic Torii rat.

  title={Increased fat absorption and impaired fat clearance cause postprandial hypertriglyceridemia in Spontaneously Diabetic Torii rat.},
  author={Tomohiko Sasase and Hisayo Morinaga and Hiromi Yamamoto and Naoto Ogawa and Kenichi Matsui and Katsuhiro Miyajima and Takashi Kawai and Yasuko Mera and Taku Masuyama and Masami Shinohara and Takeshi Ohta and Mutsuyoshi Matsushita},
  journal={Diabetes research and clinical practice},
  volume={78 1},

Acute hypertriglyceridemia promotes intestinal lymphatic lipid and drug transport: a positive feedback mechanism in lipid and drug absorption.

The data suggest that the changes to intestinal TRL formation that result from raised systemic TRL levels may impact on the absorption of highly lipophilic drugs and therefore the reproducibility of drug treatments.

Intestinal lipid absorption and transport in type 2 diabetes

Postprandial hyperlipidaemia is reduced by metformin, pioglitazone, alpha-glucosidase inhibitors, dipeptidyl peptidase 4 inhibitors and GLP-1 agonists, which reduce chylomicron production significantly in individuals with type 2 diabetes and have a direct effect on the intestine by reducing the expression of genes involved in intestinal lipoprotein metabolism.

Glucose and Lipid Metabolism in Spontaneously Diabetic Torii Rat

The characteristics of lipid metabolism in SDT rat can be useful in studies of diabetic hypertriglyceridemia and TG metabolism, and abnormality in triglyceride (TG) absorption and impaired lipid catabolism antecedent to hypoinsulinemia/hyperglycemia seem to cause postprandial hypertrigenidemia inSDT rat.

Intestinal lipoprotein overproduction in insulin-resistant states

Currently available evidence in humans and animal models strongly favors the concept that the small intestine is not merely an absorptive organ but rather plays an active role in regulating the rate of production of triglyceride-rich lipoproteins.

Key intestinal genes involved in lipoprotein metabolism are downregulated in dyslipidemic men with insulin resistance[S]

Data indicate that IR is associated with intestinal overproduction of lipoproteins and significant downregulation of key intestinal genes involved in lipid/lipoprotein metabolism.

Postprandial dyslipidemia in insulin resistant states in adolescent populations

The metabolic syndrome is discussed, focusing on the link between insulin resistance, postprandial dyslipidemia, and CVD risk, and the clinical significance and functional assessment of postpr andial dys Lipidemia in the adolescent population is discussed in more detail.

Nutrient-driven incretin secretion into intestinal lymph is different between diabetic Goto-Kakizaki rats and Wistar rats.

After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal.

Characteristics of Diabetes in the SDT Rat

The Spontaneously Diabetic Torii rat is a useful animal model of type 2 diabetes mellitus without obesity and has the potential contributions of hepatic insulin resistance and low energy expenditure to the development of diabetes.

Non-Obese Type 2 Diabetic Rat Models-GK Rat and SDT Rat

The Goto-Kakizaki rat and the Spontaneously Diabetic Torii rat are genetic non-obese type 2 diabetic models and the both rats are considered to be suitable models for investigating the etiology of the depletion of insulin secretion and impaired glucose tolerance.

Gut triglyceride production.



Role of small intestine in pathogenesis of hyperlipidemia in diabetic rats.

Investigation of whether intestinal triglyceride production utilizing endogenous substrates contributes to the pathogenesis of hyperlipidemia in diabetes found that during fasting diabetic rats have a greater than twofold increase in triglyceride output that is carried mainly by very low-density lipoproteins (VLDL).

Triglyceride Metabolism in the Alloxan-Diabetic Rat

Findingsicate that insulin withdrawal in the alloxan diabetic rat results in delayed clearing of intravenously administered chylomicrons from blood, which may be related in part to the defective uptake by adipose tissue which becomes depleted of lipoprotein lipase.

Mechanisms for development of diabetic hypertriglyceridemia in streptozotocin-treated rats. Effect of diet and duration of insulin deficiency.

It was postulated that the hypertriglyceridemia in chronically insulin-deficient rats is due entirely to a defect in lipoprotein removal, involving both dietary and endogenous fat.

Chylomicron and Chylomicron Remnant Metabolism in STZ-Induced Diabetic Rats

With affinity chromatography, it was found that the increase in serum triglycerides levels in diabetic rats was due to triglyceride-rich very-low-density lipoproteins and/or CM and not to the accumulation of remnants, which supports the observation that remnant clearance is not impaired.

Intestinal Very Low Density Lipoprotein Secretion in Insulin-deficient Rats

Although the intestine contributes a relatively small amount of VLDL-TG to the plasma pool in control and severely diabetic rats, it appears to be a significant source of very low density lipoprotein–triglyceride (VLDL) in animals with moderate insulin deficiency.

The Role of microsomal triglyceride transfer protein and dietary cholesterol in chylomicron production in diabetes

The study shows that microsomal triglycerol transfer protein mRNA is raised in diabetes without an increase in apolipoprotein B48 in the lymph suggesting that micromolecular triglyceride transfer protein regulates chylomicron triglyceride content but not particle number.

Production of Chylomicron-like Lipoproteins from Endogenous Lipid by the Intestine and Liver of Diabetic Dogs

As the hypertriglyceridemia developed in fasted dogs who had previously been on fat-free diets, the triglyceride fatty acids (TGFA) were nondietary, and the lipoproteins in these diabetic dogs resembled chylomicrons in their electrophoretic mobility, size, density, and composition.

Lipoprotein composition as a component in the lipoprotein clearance defect in experimental diabetes.

The data suggest that in addition to depressed lipoprotein lipase activity in the tissue from diabetic rats, there are also major compositional changes in circulating lipoproteins which may contribute to defective triglyceride clearance from the circulation.