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why do patients with diabetes mellitus develop hyperlipidemia

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 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 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 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 Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient.

The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity.

These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels.

The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.

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