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Hepsin enhances liver metabolism and inhibits adipocyte browning in mice.


ABSTRACT: Hepsin is a transmembrane serine protease primarily expressed in the liver. To date, the physiological function of hepsin remains poorly defined. Here we report that hepsin-deficient mice have low levels of blood glucose and lipids and liver glycogen, but increased adipose tissue browning and basal metabolic rates. The phenotype is caused by reduced hepatocyte growth factor activation and impaired Met signaling, resulting in decreased liver glucose and lipid metabolism and enhanced adipocyte browning. Hepsin-deficient mice exhibit marked resistance to high-fat diet-induced obesity, hyperglycemia, and hyperlipidemia. In db/db mice, hepsin deficiency ameliorates obesity and diabetes. These data indicate that hepsin is a key regulator in liver metabolism and energy homeostasis, suggesting that hepsin could be a therapeutic target for treating obesity and diabetes.

SUBMITTER: Li S 

PROVIDER: S-EPMC7275763 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Hepsin enhances liver metabolism and inhibits adipocyte browning in mice.

Li Shuo S   Peng Jianhao J   Wang Hao H   Zhang Wei W   Brown J Mark JM   Zhou Yiqing Y   Wu Qingyu Q  

Proceedings of the National Academy of Sciences of the United States of America 20200513 22


Hepsin is a transmembrane serine protease primarily expressed in the liver. To date, the physiological function of hepsin remains poorly defined. Here we report that hepsin-deficient mice have low levels of blood glucose and lipids and liver glycogen, but increased adipose tissue browning and basal metabolic rates. The phenotype is caused by reduced hepatocyte growth factor activation and impaired Met signaling, resulting in decreased liver glucose and lipid metabolism and enhanced adipocyte bro  ...[more]

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