Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Abstract

Hypertriglyceridaemia (HTG) is a risk factor for cardiovascular disease (CVD) in type 2 diabetes and is caused by the interaction of genes and non-genetic factors, specifically poor glycaemic control and obesity. In spite of statin treatment, residual risk of CVD remains high in type 2 diabetes, and this may relate to HTG and atherogenic dyslipidemia. Treatment of HTG emphasises correcting secondary factors and adverse lifestyles, in particular, diet and exercise. Pharmacotherapy is also required in most type 2 diabetic patients. Statins are the first-line therapy to achieve recommended therapeutic targets of plasma low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol. Fibrates, ezetimibe and n-3 fatty acids are adjunctive treatment options for residual and persistent HTG. Evidence for the use of niacin has been challenged by non-significant CVD outcomes in two recent large clinical trials. Further investigation is required to clarify the use of incretin-based therapies for HTG in type 2 diabetes. Extreme HTG, with risk of pancreatitis, may require insulin infusion therapy or apheresis. New therapies targeting HTG in diabetes need to be tested in clinical endpoint trials. The purpose of this review is to examine the current evidence and provide practical guidance on the management of HTG in type 2 diabetes.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Diabetes; Triglyceride; TherapyCore tip: Diabetic dyslipidemia relates collectively to hyperglycaemia, insulin resistance, hyperinsulinaemia, abdominal visceral adipose disposition, increased liver fat content, and dysregulated fatty acid metabolism. Insulin resistance in diabetes induces hypertriglyceridaemia by increasing the enterocytic production of chylomicrons and an impaired clearance capacity is also involved. Usual care for diabetic dyslipidemia is statin treatment, but a significant proportion of patients have residual dyslipidemia, related to hypertriglyceridaemia and atherogenic dyslipidemia. Current evidence supports the use of fenofibrate in type 2 diabetics with high triglyceride levels.Pang J, Chan DC, Watts GF. Origin and therapy for hypertriglyceridaemia in type 2 diabetes.

Cordyceps militaris Treatment Preserves Renal Function in Type 2 Diabetic Nephropathy Mice

“…Enhanced triglycerides, serum LDL, total cholesterol, and reduced HDL have also been described as characteristic alterations in diabetic patients posing a major risk factor for cardiovascular events [26, 61–63]. Our results demonstrated that CmNo1 significantly attenuated triglycerides, LDL and TC while escalated the HDL levels in DN mice suggesting their anti-atherosclerotic action (Fig 7) [50].…”

Endocrine diseases as causes of secondary hyperlipidemia

“…The TG level is further augmented by the loss of activity in LPL due to increased production of apoCIII (a physiological inhibitor of LPL). What is more, due to alterations in lipid transfer by CETP, LDL cholesterol particles in those patients become very atherogenic -"small dense LDLs" [16]. Finally, in patients with significantly elevated glycaemia, an ongoing glycation and oxidation of lipoproteins is responsible for the acceleration of atherosclerosis and its complications [17].…”

Role of the Gut in Diabetic Dyslipidemia

“…CMs and liver-derived very-low-density lipoproteins (VLDL) compete for delipidation by lipoprotein lipase (LPL) and for subsequent saturable hepatic remnant removal (5,6). In IR, lipoprotein clearance is diminished, in part due to decreased LPL activity, altered lipoprotein composition, reduced hepatic clearance and remnant removal or increased TRL pool size resulting in more competition for clearance (7). In addition, insulin mediated activation of LDLR-related protein-1 which is involved in CM remnant clearance is blunted in insulin-resistant mice (8).…”