lipoprotein lipase is activated by insulin - therefore insulin resistance and/or insulin deficiency may result in extremely elevated triglyceride levels (occasionally more than 100 mmol/L); diabetic patients who develop extremely high levels of triglycerides may already have a pre-existing partial defect in triglyceride catabolism e.g. apo E2 homozygote - in this case may also develop striate palmar xanthomata and tuberoeruptive xanthomata
if glycaemic control is reasonable and hypertriglyceridaemia is still present then this is due to an overproduction of VLDL by the liver
increased levels of non-esterified fatty acids (NEFA) are released if there is an increased quantity of adipose tissue (obesity) which often occurs in type II diabetes - this in turn probably leads to increased VLDL production
hormone-sensitive lipase (within adipocytes) is inhibited by insulin (this hydrolyses triglyceride to produce NEFA and glycerol); therefore in insulin deficiency/resistance increased levels of NEFA are released from adipocytes; also there will be lowered levels triglyceride clearance as a result of reduced activation of lipoprotein lipase
insulin has a direct inhibitory effect on VLDL production by hepatocytes - thus in insulin resistance and/or insulin deficiency triglyceride release by the liver will be further faciliated - note that even in insulin treated diabetes the liver is likely to be still insulin deficient because subcutaneously administered insulin reaches the liver via the systemic circulation (and not the portal vein)
type 1 diabetics are less likely to have hypertriglyceridaemia than type 2 diabetics - this is because insulin therapy is the rule in type 1 diabetes and other factors that predispose to hypertriglyceridaemia (such as diabetes, use of beta blocker and thiazides) are more common in type 2 diabetics
in the liver NEFA are either completely oxidised, partially oxidised (ketogenesis) or estirified (synthesis of triglyceride) - there is a resistance to ketogenesis in type 2 diabetics (mechanism not clearly determined) and, when liver energy requirements are met, this may predispose to triglyceride synthesis
low HDL levels often are present with hypertriglyceridaemia (especially in type 2 diabetics) - increased levels of small LDL are produced in type 2 diabetes with hypertriglyceridaemia
increased levels of remnant particles (or IDL) probably persist in both types of diabetes in comparison to non-diabetics
in the post-digestion phase insulin is normally secreted which promotes hepatic triglyceride storage and inhibits hepatic VLDL secretion
in this phase there are high levels of triglyceride rich lipoproteins
the promotion of hepatic triglyceride storage reduces demand on the triglyceride catabolic pathway involving lipoprotein lipase and the apo E receptor and thus prevents the postprandial accumulation of chylomicron remnants and IDL in the circulation
in diabetes there is a failure to suppress VLDL secretion postprandially (via insulin resistance or insulin deficiency) and this leads to increased levels of chylomicron remnant particles and IDL in the circulation
LDL and apo B levels - in type 1 diabetes are often normal or even reduced; in type 2 diabetes are, in general, increased
serum cholesterol levels are more atherogenic in diabetic patients than non-diabetic patients - this is because of the small, dense LDL associated with diabetes mellitus
HDL levels
normal or raised in type 1 diabetes
tend to be low in type 2 diabetes - may largely be due to other factors that are often more common in type 2 diabetes (e.g. obesity, smoking, hypertriglyceridaemia)
other factors may also co-exist with diabetes and hyperlipidaemia and increase cardiovascular risk e.g. hypertension, proteinuria and hyperfibrinogenaemia; if proteinuria exists then this signifies a generalised increased vascular permeability which thus allows increased rate of entry of marcomolecules (e.g. LDL) into the arterial subintima
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