Premium
Beta‐hydroxybutyrate favorably alters b‐cell survival and mitochondrial bioenergetics
Author(s) -
Sampson MaryJane,
Lathen Daniel,
Dallon Blake,
Draney Carrie,
Ray Jason,
Kener Kyle,
Parker Brian,
Witt Jeffrey,
Gibbs Jonathan,
Tessem Jeffery S.,
Bikman Benjamin T.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.883.8
Subject(s) - ketogenesis , bioenergetics , insulin resistance , islet , endocrinology , insulin , medicine , type 2 diabetes , diabetes mellitus , mitochondrion , beta cell , biology , ketone bodies , microbiology and biotechnology , metabolism
Pharmacological interventions aimed at improving outcomes in type 2 diabetes and achieving normoglycemia, 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. Additionally, limited evidence suggests states of ketogenesis may also improve b cell function in type 2 diabetics. Considering how little is known regarding the effects of ketones on b‐cell function, we sought to determine the specific effects of b‐hydroxybutyrate (bHB) on pancreatic b cell physiology and mitochondrial function. bHB treatment increased b cell survival and proliferation, while also increasing mitochondrial mass, respiration, and ATP production. Despite these improvements, we were unable to detect an increase in b‐cell or islet insulin production and secretion. Collectively, these findings have two implications. First, they indicate that b‐cells thrive in the midst of bHB, the circulating form of ketones. Second, improved mitochondrial function and proliferation may be insufficient to increase insulin production.