Original Research

β-Hydroxybutyrate improves β-cell mitochondrial function and survival

MaryJane Sampson, Daniel R. Lathen, Blake W. Dallon, Carrie Draney, Jason D. Ray, Kyle B. Kener, Brian A. Parker, Jonathan L. Gibbs, Jarom S. Gropp, Jeffery S. Tessem, Benjamin T. Bikman
Journal of Insulin Resistance | Vol 2, No 1 | a25 | DOI: https://doi.org/10.4102/jir.v2i1.25 | © 2017 MaryJane Sampson, Daniel R. Lathen, Blake W. Dallon, Carrie Draney, Jason D. Ray, Kyle B. Kener, Brian A. Parker, Jonathan L. Gibbs, Jarom S. Gropp, Jeffery S. Tessem, Benjamin T. Bikman | This work is licensed under CC Attribution 4.0
Submitted: 01 June 2017 | Published: 31 August 2017

About the author(s)

MaryJane Sampson, Department of Physiology and Developmental Biology, Brigham Young University, United States
Daniel R. Lathen, Department of Nutrition, Dietetics, and Food Science, Brigham Young University, United States
Blake W. Dallon, Department of Physiology and Developmental Biology, Brigham Young University, United States
Carrie Draney, Department of Nutrition, Dietetics, and Food Science, Brigham Young University, United States
Jason D. Ray, Department of Nutrition, Dietetics, and Food Science, Brigham Young University, United States
Kyle B. Kener, Department of Nutrition, Dietetics, and Food Science, Brigham Young University, United States
Brian A. Parker, Department of Physiology and Developmental Biology, Brigham Young University, United States
Jonathan L. Gibbs, Department of Physiology and Developmental Biology, Brigham Young University, United States
Jarom S. Gropp, Department of Physiology and Developmental Biology, Brigham Young University, United States
Jeffery S. Tessem, Department of Nutrition, Dietetics, and Food Science, Brigham Young University, United States
Benjamin T. Bikman, Department of Physiology and Developmental Biology, Brigham Young University, United States


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Abstract

Pharmacological interventions aimed at improving outcomes in type 2 diabetes and achieving normoglycaemia, including insulin therapy, are increasingly common, despite the potential for substantial side effects. Carbohydrate-restricted diets that result in increased ketogenesis have effectively been used to improve insulin resistance, a fundamental feature of type 2 diabetes. In addition, limited evidence suggests that states of ketogenesis may also improve β-cell function in type 2 diabetics. Considering how little is known regarding the effects of ketones on β-cell function, we sought to determine the specific effects of β-Hydroxybutyrate (βHB) on pancreatic β-cell physiology and mitochondrial function. βHB treatment increased β-cell survival and proliferation, while also increasing mitochondrial mass, respiration and adenosine triphosphate (ATP) production. Despite these improvements, were unable to detect an increase in β-cell or islet insulin production and secretion. Collectively, these findings have two implications. Firstly, they indicate that β-cells have improved survival and proliferation in the midst of βHB, the circulating form of ketones. Secondly, insulin secretion does not appear to be directly related to apparent improvements in mitochondrial function and cellular proliferation.

Keywords

diabetes mellitus; ketones; β-cells; mitochondria

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