Abnormal
fatty acid metabolism and
dyslipidemia play an intimate role in the pathogenesis of
metabolic syndrome and
cardiovascular diseases. The availability of
glucose and
insulin predominate as upstream regulatory elements that operate through a collection of
transcription factors to partition
lipids toward anabolic pathways. The unraveling of the details of these cellular events has proceeded rapidly, but their physiologic relevance to lifestyle modification has been largely ignored. Here we highlight the role of dietary input, specifically
carbohydrate intake, in the mechanism of metabolic regulation germane to
metabolic syndrome. The key principle is that
carbohydrate, directly or indirectly through the effect of
insulin, controls the disposition of excess dietary nutrients.
Dietary carbohydrate modulates lipolysis,
lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels. Several of these processes are the subject of intense investigation at the cellular level. We see the need to integrate these cellular mechanisms with results from
low-carbohydrate diet trials that have shown reduced cardiovascular risk through improvement in hepatic, intravascular, and peripheral processing of
lipoproteins, alterations in
fatty acid composition, and reductions in other cardiovascular risk factors, notably
inflammation. From the current state of the literature, however,
low-carbohydrate diets are grounded in basic metabolic principles and the data suggest that some form of
carbohydrate restriction is a candidate to be the preferred dietary strategy for cardiovascular health beyond weight regulation.