Regulation of Ketogenesis in Liver

Abstract

The sections in this article are: Roles of Insulin and Glucagon in Substrate Supply for Hepatic Ketogenesis Effects of Ketones on the Endocrine Pancreas and Adipose Tissue Intrahepatic Partitioning of Fatty Acids Between Oxidation and Esterification Pancreatic Hormone Effects on Enzyme Substrate Availability Expression of Enzyme Activity Role of Malonyl CoA Role of Carnitine Palmitoyltransferase I Membrane Topology and Membrane‐Protein Interactions Control of Carnitine Palmitoyltransferase I over Ketogenesis: Effects of Altered Insulin Status In Vivo Monitoring of Hepatic Acyl‐CoA Partitioning Intramitochondrial Regulation of Ketogenesis Modulation of Mitochondrial 3‐Hydroxy‐3‐Methylglutaryl‐CoA Synthase Activity Examples of Physiological Conditions Involving Pancreatic Hormone Regulation of Ketogenesis General Comments

Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood "Villains" of Human Metabolism

“…In ketosis, the blood pH remains buffered within normal limits [ 5 ]. Ketone bodies have effects on insulin and glucagon secretions that potentially contribute to the control of the rate of their own formation because of antilipolytic and lipolytic hormones, respectively [ 9 ]. Ketones also have a direct inhibitory effect on lipolysis in adipose tissue [ 10 ].…”

Evidence on chronic ketosis in traditional Arctic populations

“…A second reason cited by the aforementioned authors that Arctic populations were not chronically in ketosis comes from a prevalent genetic variant of CPT1A known as the Arctic variant. The CPT1A enzyme is required for transporting fatty acids into liver mitochondria for oxidation and is thus on the critical path for hepatic ketogenesis (Zammit 2011). The variant, found in Arctic populations worldwide (Collins et al 2010, Gessner et al 2011, Clemente et al 2014, has been found to reduce CPT1A activity from 2-54% (average 22%) (Collins et al 2010).…”