Measuring ketone bodies for the monitoring of pathologic and therapeutic ketosis

Joseph C Anderson, Samer G Mattar, Frank L Greenway, Richard J Lindquist, Joseph C Anderson, Samer G Mattar, Frank L Greenway, Richard J Lindquist

Abstract

Background: The ketone bodies β-hydroxybutyrate (BOHB) and acetone are generated as a byproduct of the fat metabolism process. In healthy individuals, ketone body levels are ∼0.1 mM for BOHB and ∼1 part per million for breath acetone (BrAce). These levels can increase dramatically as a consequence of a disease process or when used therapeutically for disease treatment. For example, increased ketone body concentration during weight loss is an indication of elevated fat metabolism. Ketone body measurement is relatively inexpensive and can provide metabolic insights to help guide disease management and optimize weight loss.

Methods: This review of the literature provides metabolic mechanisms and typical concentration ranges of ketone bodies, which can give new insights into these conditions and rationale for measuring ketone bodies.

Results: Diseases such as heart failure and ketoacidosis can affect caloric intake and macronutrient management, which can elevate BOHB 30-fold and BrAce 1000-fold. Other diseases associated with obesity, such as brain dysfunction, cancer, and diabetes, may cause dysfunction because of an inability to use glucose, excessive reliance on glucose, or poor insulin signaling. Elevating ketone body concentrations (e.g., nutritional ketosis) may improve these conditions by forcing utilization of ketone bodies, in place of glucose, for fuel. During weight loss, monitoring ketone body concentration can demonstrate program compliance and can be used to optimize the weight-loss plan.

Conclusions: The role of ketone bodies in states of pathologic and therapeutic ketosis indicates that accurate measurement and monitoring of BOHB or BrAce will likely improve disease management. Bariatric surgery is examined as a case study for monitoring both types of ketosis.

Keywords: acetone; bariatric surgery; metabolism; β‐hydroxybutyrate.

Conflict of interest statement

Joseph C. Anderson consults for and holds stock in Medamonitor. Samer G. Mattar has no conflicts to report. Frank L. Greenway​ reports serving on science advisory boards for JC USA, Regeneron Pharmaceuticals, and Pfizer; consulting for Jazz Pharmaceuticals, Basic Research, Dr. Reddy's Laboratories, General Nutrition Corporation, Melior Discovery Inc., Novmeta Pharma, Novo Nordisk; grants from Melior Discoveries, Novmeta Pharma; and stock/stock options from Ketogenic Health Systems, Inc., Plensat Inc., UR Labs. Richard J. Lindquist consults for Medamonitor.

© 2021 The Authors. Obesity Science & Practice published by World Obesity and The Obesity Society and John Wiley & Sons Ltd.

Figures

FIGURE 1
FIGURE 1
Acetoacetate, formed primarily from β‐oxidation of fatty acids, can be reduced to β‐hydroxybutyrate (BOHB) or decarboxylated to acetone. Beta‐hydroxybutyrate dehydrogenase (BDH) interconverts acetoacetate and BOHB depending on intercellular conditions (e.g., NADH). Acetone is produced via spontaneous or catalytic decarboxylation of acetoacetate. NADH, nicotinamide adenine dinucleotide
FIGURE 2
FIGURE 2
Pathway for utilization of ketone bodies (ketolysis) where deficiencies in SCOT or ACAT1 cause significant ketonemia (adapted from Aubert et al.67). β‐oxidation is output from β‐oxidation of fatty acids. ACAT1, acetyl‐CoA acetyltransferase1; BDH, β‐hydroxybutyrate dehydrogenase; MCT, monocarboxylate transporter; SCOT, succinyl‐CoA:3‐oxoacid‐CoA transferase

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