"Insulin induces HMG-CoA reductase activity, whereas glucagon downregulates it.[13] While glucagon production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate. The rise of insulin is, in general, determined by the digestion of carbohydrates into glucose and subsequent increase in serum glucose levels. In non-diabetics, glucagon levels are very low when insulin levels are high; however, those who have become diabetic no longer suppress glucagon output after eating.
A ketogenic diet may have similar response to taking niacin (lowered LDL and increased HDL) through beta-hydroxybutyrate, a ketone body, coupling the niacin receptor (HM74A).[10]
Lowering the blood lipid concentration of triglycerides helps lower the concentration of LDL particles, because VLDL particles converted in the bloodstream into LDL particles.[vague]
Fructose, a component of sucrose as well as high-fructose corn syrup, upregulates lilhepatic VLDL synthesis.[14]"
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