Children’s Nutrition Research Center Staff Publications

Language

English

Publication Date

11-1-2022

Journal

Journal of Clinical Investigation

DOI

10.1172/JCI152961

PMID

36107630

PMCID

PMC9621133

PubMedCentral® Posted Date

11-1-2022

PubMedCentral® Full Text Version

Post-print

Abstract

BACKGROUND

Cytochrome P450 family 8 subfamily B member 1 (CYP8B1) generates 12α-hydroxylated bile acids (BAs) that are associated with insulin resistance in humans.

METHODS

To determine whether reduced CYP8B1 activity improves insulin sensitivity, we sequenced CYP8B1 in individuals without diabetes and identified carriers of complete loss-of-function (CLOF) mutations utilizing functional assays.

RESULTS

Mutation carriers had lower plasma 12α-hydroxylated/non–12α-hydroxylated BA and cholic acid (CA)/chenodeoxycholic acid (CDCA) ratios compared with age-, sex-, and BMI-matched controls. During insulin clamps, hepatic glucose production was suppressed to a similar magnitude by insulin, but glucose infusion rates to maintain euglycemia were higher in mutation carriers, indicating increased peripheral insulin sensitivity. Consistently, a polymorphic CLOF CYP8B1 mutation associated with lower fasting insulin in the AMP-T2D-GENES study. Exposure of primary human muscle cells to mutation-carrier CA/CDCA ratios demonstrated increased FOXO1 activity, and upregulation of both insulin signaling and glucose uptake, which were mediated by increased CDCA. Inhibition of FOXO1 attenuated the CDCA-mediated increase in muscle insulin signaling and glucose uptake. We found that reduced CYP8B1 activity associates with increased insulin sensitivity in humans.

CONCLUSION

Our findings suggest that increased circulatory CDCA due to reduced CYP8B1 activity increases skeletal muscle insulin sensitivity, contributing to increased whole-body insulin sensitization.

FUNDING

Biomedical Research Council/National Medical Research Council of Singapore.

Keywords

Humans, Steroid 12-alpha-Hydroxylase, Insulin Resistance, Insulin, Haploinsufficiency, Bile Acids and Salts, Cholic Acid, Glucose, Endocrinology, Insulin signaling

Published Open-Access

yes

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