Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes

Abstract

Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) have been found to be associated with postprandial hypertriglyceridemia (PPHTg). However, whether PPHTg can cause IR and diabetes is not clear. We therefore investigated the role of PPHTg in development of T2DM in rat model of T2DM. 96 male Wistar rats were randomized into four groups (24 rats each). Control Group A, high sucrose diet (HSD) Group B, HSD+Pioglitazone (10mg/kg/day) Group C and HSD+Atorvastatin (20mg/kg/day) Group D. Fat and glucose tolerance tests were done at regular intervals in all groups besides insulin and body weight measurement. At 26 weeks, low dose streptozotocin (15mg/kg,i.p.) was given to half of the rats. All rats were followed up till 48 weeks. PPHTg developed as early as week 2 in Group B and stabilized by week 14. Group B displayed highest PPHTg compared to other groups. Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg. Group B with highest PPHTg showed highest subsequent IR, glucose intolerance (GI) and highest incidence of prediabetes at week 26 and diabetes at week 34 and 46 compared to other groups. Group D rats displayed lower IR, GI, low incidence of prediabetes and diabetes at these time points compared to Groups B and C. ROC analysis showed that triglyceride area under the curve of each time point significantly predicts the risk of diabetes. Present study provides the evidence that PPHTg predicts the development of IR, GI and T2DM in rat model of diet induced T2DM.

Association of postprandial triglyceride responses with insulin resistance among rotational night shift healthcare workers

“…Given that this is a cross‐sectional study, a cause–effect relationship of the phenomenon cannot be concluded. However, earlier studies (Aslam et al., ; Zuo et al., ) show that it is more likely that altered PPTG metabolism leads to insulin resistance and not vice versa, suggesting that the PPTG burden might be an important driver of insulin resistance among healthcare workers with rotational night shift duties. The high levels of PPTGs in the circulation result in deposition of triglycerides in ectopic sites, including the liver and muscles.…”

“…Postprandial hypertriglyceridaemia (PPHTG) is now recognized as an independent cardiovascular risk marker after being reported to have a strong association with early markers of atherosclerosis, such as carotid intima–media thickness (Boquist et al., ; Karpe et al., ; Ryu et al., ; Teno et al., ) and endothelial dysfunction (Bae et al., ; Lieberman et al., ) in non‐diabetic (Boquist et al., ; Ceriello et al., ; Karpe et al., ; Ryu et al., ) ands diabetic (Boquist et al., ; Ceriello et al., ; Karpe et al., ; Ryu et al., ; Teno et al., ) subjects. Moreover, recent research shows that PPHTG might be associated with development of insulin resistance and type 2 diabetes mellitus (Aslam, Aggarwal, Sharma, Galav, & Madhu, ; Zuo et al., ). The resultant ectopic deposition of excess triglycerides in the liver, pancreas, skeletal muscles and kidneys and consequent lipotoxic effects on these tissues result in insulin resistance and β‐cell dysfunction (Kim, Park, Hwang, Lee, & Cho, ).…”

Raspberries Improve Postprandial Glucose and Acute and Chronic Inflammation in Adults with Type 2 Diabetes

“…Postprandial elevations of glucose and triglycerides (TGs), as well as biomarkers of oxidative damage and inflammation have been associated with increased risk for CVD [4][5][6]. Postprandial hyperglycemia, hypertriglyceridemia, and concomitant systemic inflammation have also been shown to elevate risks of vascular complications in T2D [7,8].…”

Postprandial triglyceride-rich lipoproteins promote lipid accumulation and apolipoprotein B-48 receptor transcriptional activity in human circulating and murine bone marrow neutrophils in a fatty acid-dependent manner

“…New insights in epidemiology, genetic studies and biology into potential mechanisms strongly suggest that nonfasting (postprandial) triglyceride‐rich lipoproteins (TRLs) represent causal risk factor for atherosclerotic cardiovascular disease and all‐cause mortality . Accumulation of TRLs in the postprandial state occurs by overproduction and/or decreased catabolism of TRLs and is a consequence of predisposing genetic variations and medical conditions such as obesity, insulin resistance and type 2 diabetes mellitus . In healthy subjects, accumulation of TRLs in the postprandial state can also occur after the ingestion of high‐triglyceride meals .…”