PubMed · 17022532
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Toshihiko Ishida, Koji Murao. 2006-09-28. [Ectopic insulin secretion].. https://pubmed.ncbi.nlm.nih.gov/17022532/
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Involvement of novel PKCs (nPKCs) in the negative regulation of insulin-signaling pathway is a current interest of many workers investigating the cause for insulin resistance and type 2 diabetes. Free fatty acids (FFAs) are recently shown to be the major players in inducing insulin resistance in insulin target cells. They are also found to be involved in activating nPKCs associated with the impairment of insulin sensitivity. In this overview, we describe PKC delta, theta and epsilon linked to the FFA induced damage of insulin-signaling molecules.
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OBJECTIVE: To review the evidence for and against the role of visceral adipose tissue as a major contributor to the metabolic complications of obesity through abnormal regulation of lipolysis. RESEARCH METHODS AND PROCEDURES: Data from investigators in the field who have studied visceral adiposity and metabolic health and/or regional and systemic free fatty acid (FFA) release were considered. RESULTS: Although visceral fat mass was positively correlated with adverse health consequences and excess FFA availability, visceral fat was not the source of excess systemic FFA availability. Upper body non-visceral fat contributes the majority of FFAs in lean, obese, diabetic, and non-diabetic humans. Increasing amounts of visceral fat probably result in greater hepatic FFA delivery. DISCUSSION: Systemic, as opposed to hepatic, insulin resistance is unlikely to be caused by high rates of visceral adipose tissue lipolysis.