Overweight in mice and enhanced adipogenesis in vitro are associated with lack of the hedgehog coreceptor BOC

Hye Jin Lee, Shin Bum Jo, Anthony I. Romer, Hyo Jeong Lim, Min Jung Kim, Seung Hoi Koo, Robert S. Krauss, Jong Sun Kang

    Research output: Contribution to journalArticlepeer-review

    15 Citations (Scopus)

    Abstract

    Obesity arises from a combination of genetic, environmental, and behavioral factors. However, the processes that regulate white adipose tissue (WAT) expansion at the level of the adipocyte are not well understood. The Hedgehog (HH) pathway plays a conserved role in adipogenesis, inhibiting fat formation in vivo and in vitro, but it has not been shown that mice with reduced HH pathway activity have enhanced adiposity. We report that mice lacking the HH coreceptor BOC displayed age-related overweight and excess WAT. They also displayed alterations in some metabolic parameters but normal food intake. Furthermore, they had an exacerbated response to a high-fat diet, including enhanced weight gain and adipocyte hypertrophy, livers with greater fat accumulation, and elevated expression of genes related to adipogenesis, lipid metabolism, and adipokine production. Cultured Boc-/- mouse embryo fibroblasts showed enhanced adipogenesis relative to Boc+/+ cells, and they expressed reduced levels of HH pathway target genes. Therefore, a loss-of-function mutation in an HH pathway component is associated with WAT accumulation and overweight in mice. Variant alleles of such HH regulators may contribute to WAT accumulation in human individuals with additional genetic or lifestyle-based predisposition to obesity.

    Original languageEnglish
    Pages (from-to)2092-2103
    Number of pages12
    JournalDiabetes
    Volume64
    Issue number6
    DOIs
    Publication statusPublished - 2015 Jun

    Bibliographical note

    Publisher Copyright:
    © 2015 by the American Diabetes Association.

    ASJC Scopus subject areas

    • Internal Medicine
    • Endocrinology, Diabetes and Metabolism

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