Diabetic Hypertriglyceridemia Research Articles

Diabetic hypertriglyceridaemia and Alzheimer's disease: causal or not?

To summarize recent findings considering type II diabetes, or metabolic syndrome dyslipidaemia with risk for Alzheimer's disease. Population, genetic, clinical and preclinical studies support the hypothesis of increased risk for Alzheimer's disease in type 2 diabetes mellitus. The mechanisms are unclear. However, recent studies suggest that aberrations in the peripheral metabolism of triglyceride-rich-lipoproteins compromise the brain microvasculature. We review the literature of prediabetic metabolic syndrome and type 2 diabetes mellitus as a risk factor for Alzheimer's disease. We focus on a potential association with aberrations in the systemic metabolism of triglyceride-rich-lipoproteins reported over 18 months.

Moringa oleifera Lam. in Diabetes Mellitus: A Systematic Review and Meta-Analysis.

Plant-derived phytochemicals have been interested in as nutraceuticals for preventing the onset and progress of diabetes mellitus and its serious complications in recent years. Moringa oleifera Lam. is used in vegetables and in herbal medicine for its health-promoting properties against various diseases including diabetes mellitus. This study aimed to examine an effect of Moringa oleifera on diabetic hyperglycemia and dyslipidemia by meta-analyzing the current evidence of diabetic rodent models. Peer-reviewed studies written in English from two databases, PubMed and Embase, were searched to 30 April 2021. Studies reporting blood glucose or lipid levels in diabetic rodents with and without receiving extracts of Moringa oleifera were included. Forty-four studies enrolling 349 diabetic rodents treated with extracts of Moringa oleifera and 350 diabetic controls reported blood glucose levels. The pooled effect size was −3.92 (95% CI: −4.65 to −3.19) with a substantial heterogeneity. This effect was likely to be, at least in part, modified by the type of diabetic models. Moreover, diabetic hypertriglyceridemia and hypercholesterolemia were also significantly improved in diabetic rodent models treated with Moringa oleifera.

Effect of Menopause and Hypertriglyceridemia on Lipid Transfer and Paraoxonase Activity in Diabetic Women

Introduction. The high prevalence of type 2 diabetes mellitus (DM2) and cardiovascular atherosclerotic complications are increasing in women after menopause. Studies have shown that the in vitro transfer of lipids to HDL and the determination of paraoxonase activity are robust methods to HDL functional evaluation. Objective. This study aimed at observing the difference in the paraoxonase activity and the transfer of lipids to HDL in menopause DM2-women with hypertriglyceridemia. Material and Methods. Blood samples were collected from 63 female diabetic patients with hypertriglyceridemia, matched by age group and comorbidities. The artificial nanoparticle (LDE) determined the transfer to HDL by liquid scintillation, as well the activity of paraoxonase by spectrophotometry. Results. There was a difference in paraoxonase-1 activity between the groups due to the high hypertriglyceridemia, regardless of the menopausal or non-menopausal condition. And, there was also a difference in phospholipid transfer between groups. Discussion. This study showed the presence of alterations in the activity of paraoxonase and phospholipid and cholesterol ester transfer to HDL in menopausal women groups when compared to those non-menopausal groups. Conclusion. This study showed that both diabetic hypertriglyceridemia and menopause influence the HDL metabolism, and the action of paraoxonase.

Efficacy and safety of saroglitazar in managing hypertriglyceridemia in type-2 diabetes: A meta-analysis

Background and aimsSaroglitazar is commonly used in India for managing hypertriglyceridemia in diabetes. This meta-analysis evaluated the efficacy and safety of saroglitazar in hypertriglyceridemia. MethodsElectronic databases were searched for RCTs involving diabetes patients receiving saroglitazar in intervention arm, and placebo/lipid/diabetes medication in the control arm. Primary outcome was to evaluate change in serum triglyceride and HbA1c. Secondary outcomes were to evaluate changes in other lipid parameters, glycaemia and adverse effects. Analysis for lipid and glycaemic parameters were done separately for controls receiving anti-lipid medications (statins/fibrates) [active control group (ACG)] and those receiving placebo/diabetes medications [passive control group (PCG)]. ResultsFollowing 12 weeks therapy, individuals receiving saroglitazar had significantly lower triglycerides when compared to PCG [MD -71.67 mg/dl (95% CI: −123.67 to −19.66 mg/dl); P < 0.01; I2 = 91% (considerable heterogeneity); low certainty of evidence (LCE)], but not ACG [MD -37.38 mg/dl (95% CI: −84.55–9.79 mg/dl; P = 0.12; I2 = 98% (considerable heterogeneity); LCE]. Individuals receiving saroglitazar had significantly lower fasting glucose when compared to PCG [MD -24.61 mg/dl (95% CI: −44.13 to −5.09 mg/dl); P = 0.01; I2 = 65% (moderate heterogeneity); LCE], but not ACG [MD -13.5 mg/dl (95% CI: −33.1–6.10 mg/dl; P = 0.18; I2 = 98% (considerable heterogeneity); LCE]. HbA1c, total cholesterol, LDL-C, apolipoprotein-B and HDL-C were not significantly different among study groups. Creatinine was significantly higher in patients receiving saroglitazar as compared to controls [MD 0.12 mg/dl (95% CI: 0.04–0.21 mg/dl); P < 0.01; I2 = 29% (low heterogeneity); high certainty of evidence]. ConclusionThis meta-analysis reinforces the excellent triglyceride lowering of saroglitazar, but highlights significant increase in creatinine.

Tubelight Adrenals in Diabetic Ketoacidosis.

Case PresentationWe report a patient with the triad of diabetic ketoacidosis, hypertriglyceridemia, and acute pancreatitis associated with computed tomography hypoperfusion complex and adrenal hyperdensity on abdominal imaging – an association not previously reported in diabetic ketoacidosis.DiscussionPresence of computed tomography hypoperfusion complex with hyperdense ‘Tubelight adrenals’ in a patient with diabetic ketoacidosis is associated with poor prognosis and thus serves to guide clinicians towards early and aggressive management.

1506-P: Nonalcoholic Fatty Liver Disease (NAFLD) in Type 2 Diabetes Mellitus (T2DM) Patients in India: A Real-World Perspective

Objective: NAFLD is highly prevalent in T2 DM patients. In addition to diabetes, factors like age (&amp;gt; 45 years), obesity (body mass index &amp;gt; 30 kg/m2), dyslipidemia, hypertriglyceridemia, hypertension and poor control of diabetes contribute to higher risk of having NAFLD. Therefore, the study was designed to evaluate the profile of T2DM patients with NAFLD in India alongwith determining high risk factors for having NAFLD. Methodology: Ultrasonographic (USG) records (1985) of patients with available liver function test (LFT) reports were analyzed after excluding alcoholic liver disease (ALD) and other known causes of liver injury. Various clinical and diagnostic parameters were assessed. Univariate and multivariate logistic regression was used to determine significant risk factors (P value &amp;lt;0.05). Results: Out of 1985 patients, 72.24% patients had NAFLD. Most were males (65%), &amp;gt;40 years (82.99%) and obese/overweight (92%). Most had normal SGOT (89.33%) and SGPT (74%) levels. The ratio of SGOT/SGPT was less than 1 in 77.20% patients. Most (51.62%) patients had poor control of diabetes (HbA1c &amp;gt;7.5%). Dyslipidemia and hypertriglyceridemia were seen in 80% and 48.16% patients. On univariate logistic regression analysis, age (P&amp;lt;0.001), uric acid (P&amp;lt;0.05), SGOT (P&amp;lt;0.001), SGPT (P&amp;lt;0.001), triglycerides (P&amp;lt;0.001), HDL (P&amp;lt;0.001) and LDL (P&amp;lt;0.001) levels were significantly associated. On multivariate analysis, only HDL (P&amp;lt;0.001), SGOT (P&amp;lt;0.001), SGPT (P&amp;lt;0.001) and SGOT/SGPT ratio (P&amp;lt;0.001) were significantly associated. A predictive algorithm using the above was designed and validated. Conclusion: NAFLD was seen to be highly prevalent in diabetes patients in India. Most of these patients had normal LFT values which highlight the need for routine screening and management of these patients, especially those with high risk factors. Disclosure V. Singh: None. M. Singh: None. H. Patidar: None.

Plasmapheresis for Recurrent Acute Pancreatitis from Hypertriglyceridemia

Acute pancreatitis is a known complication of severe hypertriglyceridemia. Therapeutic experience with plasmapheresis is less well reported but has been highly successful in life-threatening presentations. We describe a 38-year-old obese Hispanic woman with a previous history of acute pancreatitis from diabetic hypertriglyceridemia who presented to the emergency department with a 2-day history of worsening abdominal pain. Plasmapheresis was initiated with one calculated plasma volume exchange using 5% albumin replacement within 24 hours of admission. Following this treatment, the triglyceride level fell 74%. Another session was performed the following day. The final triglyceride level represented a 93% reduction. This case is novel in that the patient presented twice within the same year with hypertriglyceridemic pancreatitis and responded well to prompt plasmapheresis therapy.

The Prevalence of Nonalcoholic Fatty Liver Disease and Related Metabolic Comorbidities Was Associated with Age at Onset of Moderate to Severe Plaque Psoriasis: A Cross-Sectional Study.

Nonalcoholic fatty liver disease (NAFLD) has been found to be highly prevalent in psoriatic patients. Adult onset psoriasis could be divided into either early or late onset psoriasis. The associations between NAFLD and related metabolic comorbidities and age at onset of psoriasis have not yet been investigated. Our study was to evaluate the associations between prevalence of NAFLD and related metabolic conditions and early, late, and childhood onset psoriasis. A cross-sectional observational study was conducted on patients with moderate to severe plaque psoriasis. Data on clinical characteristics of NAFLD and related metabolic diseases (diabetes, hypertriglyceridemia, hyperuricemia, and metabolic syndrome) were collected. The prevalence of NAFLD in 439 patients (mean: 51±14 years, range: 18–85 years) was 55.8%. NAFLD was frequently identified in early onset patients (74.2%), and this diagnosis was particularly common in patients currently younger than 40 (85.3%). Diabetes was the least prevalent component of metabolic syndrome in early onset patients with metabolic syndrome but the most often found component in late onset ones. Patients with childhood onset psoriasis had the lowest frequencies of all metabolic comorbidities except hyperuricemia among the three groups. In the multivariate analyses, early onset was independently and positively associated with NAFLD, hypertriglyceridemia and hyperuricemia and independently and negatively associated with diabetes among early and late onset patients. The results suggested prevalence of NAFLD and related metabolic comorbidities was associated with age at onset of moderate to severe plaque psoriasis. Early onset of psoriasis was independently associated with greater odds of NAFLD, hypertriglyceridemia, hyperuricemia and smaller odds of diabetes compared to late onset. Early onset patients have metabolic syndrome mainly related to lipid disorders and abnormal glucose metabolism was not often involved.

Lipolysis, and not hepatic lipogenesis, is the primary modulator of triglyceride levels in streptozotocin-induced diabetic mice.

Diabetic hypertriglyceridemia is thought to be primarily driven by increased hepatic de novo lipogenesis. However, experiments in animal models indicated that insulin deficiency should decrease hepatic de novo lipogenesis and reduce plasma triglyceride levels. To address the discrepancy between human data and genetically altered mouse models, we investigated whether insulin-deficient diabetic mice had triglyceride changes that resemble those in diabetic humans. Streptozotocin-induced insulin deficiency increased plasma triglyceride levels in mice. Contrary to the mouse models with impaired hepatic insulin receptor signaling, insulin deficiency did not reduce hepatic triglyceride secretion and de novo lipogenesis-related gene expression. Diabetic mice had a marked decrease in postprandial triglycerides clearance, which was associated with decreased lipoprotein lipase and peroxisome proliferator-activated receptor α mRNA levels in peripheral tissues and decreased lipoprotein lipase activity in skeletal muscle, heart, and brown adipose tissue. Diabetic heterozygous lipoprotein lipase knockout mice had markedly elevated fasting plasma triglyceride levels and prolonged postprandial triglycerides clearance. Insulin deficiency causes hypertriglyceridemia by decreasing peripheral lipolysis and not by an increase in hepatic triglycerides production and secretion.

Plasmapheresis in the Management of Severe Hypertriglyceridemia

Plasmapheresis can benefit a variety of critically ill patients. A woman with diabetic ketoacidosis and severe hypertriglyceridemia was treated with plasmapheresis when conventional treatments did not markedly reduce her triglyceridemia. The patient was admitted to a medical intensive care unit because of diabetic ketoacidosis with severe lipemia. The lipemia-associated interference in laboratory studies made treatment of electrolyte abnormalities extremely difficult. The hypertriglyceridemia was initially treated with insulin, antilipidemic medications, and heparin, but the levels of triglycerides remained elevated, delaying results of needed laboratory studies for hours. After plasmapheresis, the serum level of triglycerides decreased by 77% in less than 24 hours. Severe lipemia interferes with photometric laboratory studies, yielding an underestimation of serum levels of electrolytes. Plasmapheresis is safe, rapid, and effective for emergent management of severe hypertriglyceridemia in critically ill patients. The impact of the procedure on critical care nursing is growing as nurses become involved in the treatment and follow-up care of patients who have plasmapheresis.

Apolipoprotein C-III and hepatic triglyceride-rich lipoprotein production

A strong positive correlation between plasma apolipoprotein (apo) C-III and triglyceride concentrations has been invariably observed in human and animal studies. The hypertriglyceridemic effect of apo C-III has been conventionally explained by its extracellular roles in inhibiting lipolysis catalysed by lipoprotein lipase and attenuating triglyceride-rich lipoprotein clearance through receptor-dependent and/or independent mechanisms. However, recent experimental evidence suggests that apo C-III may also play an intracellular role in promoting hepatic triglyceride-rich lipoprotein production. Kinetic studies with humans and genetically modified mice have shown that apo C-III is linked with increased production of triglyceride-rich lipoproteins, such as very-low-density lipoprotein 1 (VLDL1). Mutational studies on human apo C-III variants (originally identified in humans with hypotriglyceridemia or hyperalphalipoproteinemia) provide the structure-function analysis of human apo C-III, demonstrating that loss-of-function mutations within human apo C-III impair the assembly and secretion of triglyceride-rich VLDL1 under lipid-rich conditions. The current review summarizes recent experimental evidence for an intrahepatic role of human apo C-III in promoting mobilization and utilization of triglyceride during VLDL1 assembly/secretion. Understanding mechanisms by which hepatic apo C-III expression is regulated under insulin resistance and diabetic conditions will lead to better and more rational strategies for the prevention and treatment of diabetic hypertriglyceridemia that is closely related to premature atherosclerosis.

Glucose and Lipid Metabolism in Spontaneously Diabetic Torii Rat

The impairment of glucose metabolism may lead to type 2 diabetes and the malfunction of lipid metabolism contributing to metabolic syndrome, which increases risk of heart disease, vascular disease, and type 2 diabetes. Our previous study provided evidence for involvement of hepatic glucose metabolic disorder in onset and progress of diabetes in Spontaneously Diabetic Torii (SDT) rats. As it is increasingly important to elucidate the mechanism of onset of diabetes and to develop drugs to prevent diabetic pathological progress, SDT rat should offer a highly useful model of spontaneous diabetic onset for such studies. In addition, abnormality in triglyceride (TG) absorption and impaired lipid catabolism antecedent to hypoinsulinemia/hyperglycemia seem to cause postprandial hypertriglyceridemia in SDT rat; hence, the characteristics of lipid metabolism in SDT rat can be useful in studies of diabetic hypertriglyceridemia and TG metabolism.

Management of Hypertriglyceridemia in the Diabetic Patient

The hypertriglyceridemia of diabetes can be classified into mild to moderate (triglycerides between 150–499 mg/dL) and severe hypertriglyceridemia (triglycerides ≥500 mg/dL). As in any other individuals with hypertriglyceridemia, secondary causes need to be excluded. The management of severe hypertriglyceridemia (chylomicronemia syndrome) includes aggressive reduction of triglycerides with intravenous insulin, fibrates, omega-3 fatty acids, and/or niacin therapy to avert the risk of pancreatitis. In patients with mild to moderate hypertriglyceridemia, the treatment of choice is statin therapy to achieve the low-density lipoprotein (LDL) and non-high-density lipoprotein (HDL) target goals. The evidence base would favor niacin therapy in combination with statin therapy to achieve the goals pertaining to LDL cholesterol and non-HDL cholesterol. The data about the combination of fibrate therapy with statin therapy are disappointing.

Ruboxistaurin attenuates hypertriglyceridemia in diabetic rats: Comparison with the antioxidant N‐acetylcysteine

Hyperglycemia‐induced oxidative stress plays a critical role in the development of diabetic metabolic complications including hypertriglyceridemia. The beta isoform of Protein kinase C (PKCβ) is over‐expressed in various organs of diabetic rodents and can cause or exacerbate oxidative stress by activating NADPH oxidase, a major source of superoxide production in the cardiovascular system. We postulated that selective PKCβ inhibition with ruboxistaurin (RXT) may attenuate hypertriglyceridemia in diabetes by reducing oxidative stress. Control or streptozotozin‐induced diabetic rats were either untreated (C, D) or treated with RXT (1 mg/kg/day, D+RXT) or with the antioxidant N‐acetylcycsteine (NAC) (1.5g/kg/day, D+NAC) delivered by oral gavage for four weeks. Levels of 15‐F2t‐isoprostane (IsoP), a specific marker of oxidative stress, were significantly increased in D group in both the myocardium and plasma. This was accompanied by a marked increase in plasma triglycerides (P&lt;0.05 vs. C). RXT and NAC, respectively, prevented the increase of IsoP and significantly attenuated the increases of triglycerides. However, triglycerides in the D+NAC group was lowered further than that in the D+RXT group (P&lt;0.05). Despite similar antioxidant properties, ruboxistaurin seems to be inferior to NAC in reducing hypertriglyceridemia in diabetes.Supported by RGC/GRF grants (781109 M to ZX, 766709 M to MGI).

A case of acute pancreatitis induced by hypertriglyceridemia in gestational diabetes

Hypertriglyceridemia is a rare cause of pancreatitis in pregnancy. Pregnancy is related with hypertriglyceridemia especially in the 3rd trimester due to increase of estrogen. Diabetes is known as a common cause of secondary lipid metabolism disorder and is often associated with hypertriglyceridemia. Shock and sepsis related to pancreatitis in pregnancy result in a relatively high morbidity and mortality rate for both the mother and the fetus. Hypertriglyceridemic pancreatitis complicated in gestational diabetes has not previously been reported. We report a case of 26 +4 weeks gestational aged primigravida with acute pancreatitis induced by hypertriglyceridemia in gestational diabetes. We reviewed the clinical courses and treatments of acute pancreatitis in pregnancy with the literatures.

Clinical Profile and Etiology of Diabetes Mellitus With Onset at Less Than 6 Months of Age

The aim of this study was to determine the clinical profile and etiology of diabetes mellitus (DM) with onset at < 6 months of age. All children aged < 6 months diagnosed with DM at a tertiary referral center between 2005 and 2008 were included in the study. Three cases of DM with onset at < 6 months of age were identified. All patients were female and of the same ethnic origin, with nonconsanguineous parents. Intrauterine growth retardation was noted in all three patients, and diabetic ketoacidosis and hypertriglyceridemia in two of the three. Blood samples from all three patients and their parents were analyzed for mutations in the KCNJ11 gene (inwardly-rectifying potassium channel, subfamily J, member 11 gene; OMIM 600937). A heterozygous de novo mutation in the KCNJ11 gene was detected in one patient, which confirmed the diagnosis of permanent neonatal DM. Neither C-peptide secretion nor circulating islet cell antibodies were detected in any patient during diagnosis, but C-peptide elevation was detected in the patient with permanent neonatal DM after treatment with sulfonylurea. One infant had clinical and immunological evidence of congenital cytomegalovirus infection while the diabetes in another case was postulated to be syndromic. DM within the first 6 months of life is a rare condition with various etiologies. The high prevalence of Kir6.2 mutations in neonatal diabetes means that all children < 6 months of age diagnosed with diabetes should be tested for Kir6.2 mutations at diagnosis.

The APOA5−1131 T > C variant enhances the association between RBP4 and hypertriglyceridemia in diabetes

Background and aim Type 2 diabetic patients have an increased prevalence of hypertriglyceridemia. RBP4 has been associated with insulin resistance and hypertriglyceridemia in obesity, the metabolic syndrome and type 2 diabetes. APOA5 is proposed to be a genetic modulator of triglycerides. The aim of this study was to evaluate the relationship between RBP4 plasma levels and lipid disturbances and to determine the impact of the APOA5−1131 T > C variant on this relationship in type 2 diabetic patients. Methods and results A total of 165 type 2 diabetic patients were included in the study. RBP4 plasma levels and the APOA5−1131 T > C variant were determined and the complete lipid profile was assessed by sequential ultracentrifugation. RBP4 was positively correlated with triglyceride levels in plasma and with all the components of triglyceride-rich lipoproteins. Despite the fact that a statistically significant relationship between the APOA5 genetic variant and RBP4 plasma levels was not found, the hypertriglyceridemic effect of high RBP4 levels was enhanced by the presence of the APOA5−1131 T > C genetic variant. Correlation coefficients were 2-fold higher for TC carriers compared to TT carriers with regard to RBP4 plasma levels and all the components of triglyceride-rich lipoproteins. Those type 2 diabetic patients with high RBP4 plasma concentrations and who were TC carriers showed an increased incidence of hypertriglyceridemia (OR = 7.46, P = 0.010). Conclusion RBP4 is associated with hypertriglyceridemia in type 2 diabetic patients. The RBP4 effect is conditioned by the presence of the APOA5−1131 T > C genetic variant.

EFFECT OFCUCURBITA FICIFOLIAFRUIT EXTRACT ON LIPID PROFILE AND ORAL GLUCOSE TOLERANCE IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

ABSTRACT Cucurbita ficifolia (C. ficifolia) commonly known as pumpkin is a cultivated plant whose fruit can be used for treating various diseases, one of which is diabetes mellitus. This study was undertaken to investigate the effects of long term feeding of C. ficifolia fruit extract on blood glucose, lipid profiles and the oral glucose tolerance test in streptozotocin (STZ)-induced type 1 diabetic rats. Treatment for 30 days showed a significant decrease in blood glucose, triglyceride, low density lipoprotein and a significant increase in high density lipoprotein level. A significant effect on oral glucose tolerance was also noted. Chronic administration showed an improvement in the oral glucose tolerance curve. These results suggest that C. ficifolia fruit extract exhibits hypoglycemic as well as hypolipidemic effects in the STZ-induced diabetic rats. PRACTICAL APPLICATIONS Cucurbita ficifolia, also referred to as pumpkin, is commonly used as a traditional remedy for diabetes in Asia, Africa and South America. The present study investigated the hypoglycemic and hypolipidemic effects of C. ficifolia fruit extract in rats with streptozotocin-induced experimental diabetes. Findings from this study demonstrate that C. ficifolia fruit extract has been shown to have, besides hypoglycemic properties, strong hypolipidemic action on diabetic hypertriglyceridemia and hypercholesterolemia as well. Therefore, consumption of C. ficifolia fruit as a therapeutic diet may be useful in the treatment of diabetes.

FoxO1 mediates insulin-dependent regulation of hepatic VLDL production in mice

Excessive production of triglyceride-rich VLDL is attributable to hypertriglyceridemia. VLDL production is facilitated by microsomal triglyceride transfer protein (MTP) in a rate-limiting step that is regulated by insulin. To characterize the underlying mechanism, we studied hepatic MTP regulation by forkhead box O1 (FoxO1), a transcription factor that plays a key role in hepatic insulin signaling. In HepG2 cells, MTP expression was induced by FoxO1 and inhibited by exposure to insulin. This effect correlated with the ability of FoxO1 to bind and stimulate MTP promoter activity. Deletion or mutation of the FoxO1 target site within the MTP promoter disabled FoxO1 binding and resulted in abolition of insulin-dependent regulation of MTP expression. We generated mice that expressed a constitutively active FoxO1 transgene and found that increased FoxO1 activity was associated with enhanced MTP expression, augmented VLDL production, and elevated plasma triglyceride levels. In contrast, RNAi-mediated silencing of hepatic FoxO1 was associated with reduced MTP and VLDL production in adult mice. Furthermore, we found that hepatic FoxO1 abundance and MTP production were increased in mice with abnormal triglyceride metabolism. These data suggest that FoxO1 mediates insulin regulation of MTP production and that augmented MTP levels may be a causative factor for VLDL overproduction and hypertriglyceridemia in diabetes.

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

In diabetes, postprandial hyperlipidemia is recognized as a risk factor for premature atherosclerosis and following cardiovascular disease. In the present study, features of fat absorption and clearance were examined to clarify the lipid metabolism of Spontaneously Diabetic Torii (SDT) rats. Olive oil was orally administered to evaluate increase of blood triglyceride (TG) level. Mesenteric lymph chylomicron TG was also measured. mRNAs of enzymes and transfer protein related to TG metabolism and histopathological changes were evaluated. In an oil loading test, elevation of TG in plasma and lymph chylomicron was increased in SDT rats. Interestingly, SDT rats showed elevation of plasma TG after oil loading and relatively low epididymal fat lipoprotein lipase (LPL) mRNA expression even at the pre-diabetic state without increase of TG absorption from intestine. In the diabetic state, intestines of SDT rats were hypertrophic and expressed mRNAs of enzymes and transfer protein related to TG absorption highly. From these results, it seems that intestinal abnormalities related to hypoinsulinemia/hyperglycemia cause postprandial hypertriglyceridemia in SDT rats. In addition, our findings suggest that SDT rats have impaired lipid catabolism antecedent to hypoinsulinemia/hyperglycemia. These characteristics of SDT rats can be useful in studies of diabetic hypertriglyceridemia and TG metabolism.