INPP4B protects from metabolic syndrome and associated disorders

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

INPP4B protects from metabolic syndrome and associated disorders. / Zhang, Manqi; Ceyhan, Yasemin; Kaftanovskaya, Elena M.; Vasquez, Judy L.; Vacher, Jean; Knop, Filip K.; Nathanson, Lubov; Agoulnik, Alexander I.; Ittmann, Michael M.; Agoulnik, Irina U.

In: Communications Biology , Vol. 4, No. 1, 416, 2021.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Zhang, M, Ceyhan, Y, Kaftanovskaya, EM, Vasquez, JL, Vacher, J, Knop, FK, Nathanson, L, Agoulnik, AI, Ittmann, MM & Agoulnik, IU 2021, 'INPP4B protects from metabolic syndrome and associated disorders', Communications Biology , vol. 4, no. 1, 416. https://doi.org/10.1038/s42003-021-01940-6

APA

Zhang, M., Ceyhan, Y., Kaftanovskaya, E. M., Vasquez, J. L., Vacher, J., Knop, F. K., Nathanson, L., Agoulnik, A. I., Ittmann, M. M., & Agoulnik, I. U. (2021). INPP4B protects from metabolic syndrome and associated disorders. Communications Biology , 4(1), [416]. https://doi.org/10.1038/s42003-021-01940-6

Vancouver

Zhang M, Ceyhan Y, Kaftanovskaya EM, Vasquez JL, Vacher J, Knop FK et al. INPP4B protects from metabolic syndrome and associated disorders. Communications Biology . 2021;4(1). 416. https://doi.org/10.1038/s42003-021-01940-6

Author

Zhang, Manqi ; Ceyhan, Yasemin ; Kaftanovskaya, Elena M. ; Vasquez, Judy L. ; Vacher, Jean ; Knop, Filip K. ; Nathanson, Lubov ; Agoulnik, Alexander I. ; Ittmann, Michael M. ; Agoulnik, Irina U. / INPP4B protects from metabolic syndrome and associated disorders. In: Communications Biology . 2021 ; Vol. 4, No. 1.

Bibtex

@article{e9cde2a664db4a14be270178a047ec44,
title = "INPP4B protects from metabolic syndrome and associated disorders",
abstract = "A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers. The causative cellular signals are multifactorial and not yet completely understood. In this report, we show that Inositol Polyphosphate-4-Phosphatase Type II B (INPP4B) signaling protects mice from diet-induced metabolic dysfunction. INPP4B suppresses AKT and PKC signaling in the liver thereby improving insulin sensitivity. INPP4B loss results in the proteolytic cleavage and activation of a key regulator in de novo lipogenesis and lipid storage, SREBP1. In mice fed with the high fat diet, SREBP1 increases expression and activity of PPARG and other lipogenic pathways, leading to obesity and non-alcoholic fatty liver disease (NAFLD). Inpp4b−/− male mice have reduced energy expenditure and respiratory exchange ratio leading to increased adiposity and insulin resistance. When treated with high fat diet, Inpp4b−/− males develop type II diabetes and inflammation of adipose tissue and prostate. In turn, inflammation drives the development of high-grade prostatic intraepithelial neoplasia (PIN). Thus, INPP4B plays a crucial role in maintenance of overall metabolic health and protects from prostate neoplasms associated with metabolic dysfunction.",
author = "Manqi Zhang and Yasemin Ceyhan and Kaftanovskaya, {Elena M.} and Vasquez, {Judy L.} and Jean Vacher and Knop, {Filip K.} and Lubov Nathanson and Agoulnik, {Alexander I.} and Ittmann, {Michael M.} and Agoulnik, {Irina U.}",
year = "2021",
doi = "10.1038/s42003-021-01940-6",
language = "English",
volume = "4",
journal = "Communications Biology",
issn = "2399-3642",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - INPP4B protects from metabolic syndrome and associated disorders

AU - Zhang, Manqi

AU - Ceyhan, Yasemin

AU - Kaftanovskaya, Elena M.

AU - Vasquez, Judy L.

AU - Vacher, Jean

AU - Knop, Filip K.

AU - Nathanson, Lubov

AU - Agoulnik, Alexander I.

AU - Ittmann, Michael M.

AU - Agoulnik, Irina U.

PY - 2021

Y1 - 2021

N2 - A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers. The causative cellular signals are multifactorial and not yet completely understood. In this report, we show that Inositol Polyphosphate-4-Phosphatase Type II B (INPP4B) signaling protects mice from diet-induced metabolic dysfunction. INPP4B suppresses AKT and PKC signaling in the liver thereby improving insulin sensitivity. INPP4B loss results in the proteolytic cleavage and activation of a key regulator in de novo lipogenesis and lipid storage, SREBP1. In mice fed with the high fat diet, SREBP1 increases expression and activity of PPARG and other lipogenic pathways, leading to obesity and non-alcoholic fatty liver disease (NAFLD). Inpp4b−/− male mice have reduced energy expenditure and respiratory exchange ratio leading to increased adiposity and insulin resistance. When treated with high fat diet, Inpp4b−/− males develop type II diabetes and inflammation of adipose tissue and prostate. In turn, inflammation drives the development of high-grade prostatic intraepithelial neoplasia (PIN). Thus, INPP4B plays a crucial role in maintenance of overall metabolic health and protects from prostate neoplasms associated with metabolic dysfunction.

AB - A high fat diet and obesity have been linked to the development of metabolic dysfunction and the promotion of multiple cancers. The causative cellular signals are multifactorial and not yet completely understood. In this report, we show that Inositol Polyphosphate-4-Phosphatase Type II B (INPP4B) signaling protects mice from diet-induced metabolic dysfunction. INPP4B suppresses AKT and PKC signaling in the liver thereby improving insulin sensitivity. INPP4B loss results in the proteolytic cleavage and activation of a key regulator in de novo lipogenesis and lipid storage, SREBP1. In mice fed with the high fat diet, SREBP1 increases expression and activity of PPARG and other lipogenic pathways, leading to obesity and non-alcoholic fatty liver disease (NAFLD). Inpp4b−/− male mice have reduced energy expenditure and respiratory exchange ratio leading to increased adiposity and insulin resistance. When treated with high fat diet, Inpp4b−/− males develop type II diabetes and inflammation of adipose tissue and prostate. In turn, inflammation drives the development of high-grade prostatic intraepithelial neoplasia (PIN). Thus, INPP4B plays a crucial role in maintenance of overall metabolic health and protects from prostate neoplasms associated with metabolic dysfunction.

U2 - 10.1038/s42003-021-01940-6

DO - 10.1038/s42003-021-01940-6

M3 - Journal article

C2 - 33772116

AN - SCOPUS:85103562192

VL - 4

JO - Communications Biology

JF - Communications Biology

SN - 2399-3642

IS - 1

M1 - 416

ER -

ID: 259881938