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Review
, 7 (3), 97-106

Nutritional Ketosis for Weight Management and Reversal of Metabolic Syndrome

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Review

Nutritional Ketosis for Weight Management and Reversal of Metabolic Syndrome

Victoria M Gershuni et al. Curr Nutr Rep.

Abstract

Purpose of review: The goal of this paper is to review current literature on nutritional ketosis within the context of weight management and metabolic syndrome, namely, insulin resistance, lipid profile, cardiovascular disease risk, and development of non-alcoholic fatty liver disease. We provide background on the mechanism of ketogenesis and describe nutritional ketosis.

Recent findings: Nutritional ketosis has been found to improve metabolic and inflammatory markers, including lipids, HbA1c, high-sensitivity CRP, fasting insulin and glucose levels, and aid in weight management. We discuss these findings and elaborate on potential mechanisms of ketones for promoting weight loss, decreasing hunger, and increasing satiety. Humans have evolved with the capacity for metabolic flexibility and the ability to use ketones for fuel. During states of low dietary carbohydrate intake, insulin levels remain low and ketogenesis takes place. These conditions promote breakdown of excess fat stores, sparing of lean muscle, and improvement in insulin sensitivity.

Keywords: Glucose metabolism; Insulin resistance; Ketogenesis; Ketogenic diet; Ketone bodies; Low-carbohydrate diet; Metabolic syndrome; Nutritional ketosis; Weight loss.

Conflict of interest statement

Compliance with Ethics Guidelines

Conflict of Interest

Victoria M. Gershuni, Stephanie L. Yan, and Valentina Medici declare they have no conflict of interest.

Figures

Figure 1.
Figure 1.
Ketogenesis, the production of ketones for fuel, is a normal, physiologic process that occurs via hepatic beta-oxidation of free fatty acids in the mitochondria of liver cells. Energy stored as fat in adipose tissue is liberated to acetyl-CoA and converted to ketones. Extra-hepatic tissues are able to undergo ketolysis and convert ketones back to acetyl-CoA which enters the TCA cycle and is used by the mitochondria to generate ATP for energy.

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