Influence of dietary carbohydrate and fat on LDL and HDL particle distributions.

Variations in the size and density distributions of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles have been related to risk for cardiovascular disease. In particular, increased levels of small, dense LDL particles, together with reduced levels of large HDL and increases in small HDL, are integral features of the atherogenic dyslipidemia found in patients with insulin resistance, obesity, and metabolic syndrome. Increased dietary carbohydrates, particularly simple sugars and starches with high glycemic index, can increase levels of small, dense LDL and HDL, primarily by mechanisms that involve increasing plasma triglyceride concentrations.

Dyslipidemia in type 2 diabetes.

Type 2 diabetes mellitus is associated with a cluster of lipid abnormalities:elevated plasma triglycerides, reduced high-density lipoprotein cholesterol, and smaller and denser low-density lipoproteins,which have been associated with an increased risk of cardiovascular disease. Insulin resistance may contribute to dyslipidemia associated with type 2 diabetes by increasing hepatic secretion of large,triglyceride-rich very low-density lipoprotein particles and by impairing the clearance of lipoprotein particles from plasma. Lifestyle interventions may be effective in improving the diabetic dyslipidemia syndrome.

Metabolic abnormalities: triglyceride and low-density lipoprotein.

Increased plasma triglyceride and reduced high-density lipoprotein cholesterol are key features of the metabolic syndrome. Although elevated low-density lipoprotein cholesterol is not an integral characteristic of this syndrome, there is commonly an increase in the proportion of small, dense low-density lipoprotein particles. Together, these abnormalities constitute the atherogenic dyslipidemia of the metabolic syndrome.

Ovariectomy leads to increased insulin resistance in human apolipoprotein B transgenic mice lacking brown adipose tissue.

We studied the role of estrogen in the gender differences in insulin resistance observed in the apoB/BATless mouse, a model of obesity, insulin resistance, and hyperlipidemia. Ovariectomized apoB/BATless mice were more obese and more insulin-resistant than sham ovariectomized apoB/BATless mice. Estrogen replacement by subcutaneous pellet reversed the obesity, lowered plasma insulin levels, and normalized both glucose tolerance and insulin sensitivity associated with ovariectomy.