Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1

Prameladevi Chinnasamy; Isabel Casimiro; Dario F. Riascos-Bernal; Shreeganesh Venkatesh; Dippal Parikh; Alishba Maira; Aparna Srinivasan; Wei Zheng; Elena Tarabra; Haihong Zong; Smitha Jayakumar; Venkatesh Jeganathan; Kith Pradan; Jose O. Aleman; Rajat Singh; Sayan Nandi; Jeffrey E. Pessin; Nicholas E.S. Sibinga

doi:10.1038/s41467-022-35683-7

Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1

Prameladevi Chinnasamy, Isabel Casimiro, Dario F. Riascos-Bernal, Shreeganesh Venkatesh, Dippal Parikh, Alishba Maira, Aparna Srinivasan, Wei Zheng, Elena Tarabra, Haihong Zong, Smitha Jayakumar, Venkatesh Jeganathan, Kith Pradan, Jose O. Aleman, Rajat Singh, Sayan Nandi, Jeffrey E. Pessin, Nicholas E.S. Sibinga

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Recent studies implicate macrophages in regulation of thermogenic, sympathetic neuron-mediated norepinephrine (NE) signaling in adipose tissues, but understanding of such non-classical macrophage activities is incomplete. Here we show that male mice lacking the allograft inflammatory factor-1 (AIF1) protein resist high fat diet (HFD)-induced obesity and hyperglycemia. We link this phenotype to higher adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance by AIF1-deficient macrophages, and find through reciprocal bone marrow transplantation that donor Aif1^-/- vs WT genotype confers the obesity phenotype in mice. Interestingly, human sequence variants near the AIF1 locus associate with obesity and diabetes; in adipose samples from participants with obesity, we observe direct correlation of AIF1 and MAOA transcript levels. These findings identify AIF1 as a regulator of MAOA expression in macrophages and catecholamine activity in adipose tissues – limiting energy expenditure and promoting energy storage – and suggest how it might contribute to human obesity.

Original language	English (US)
Article number	38
Journal	Nature communications
Volume	14
Issue number	1
DOIs	https://doi.org/10.1038/s41467-022-35683-7
State	Published - Dec 2023

ASJC Scopus subject areas

General Chemistry
General Biochemistry, Genetics and Molecular Biology
General Physics and Astronomy

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/s41467-022-35683-7

Cite this

Chinnasamy, P., Casimiro, I., Riascos-Bernal, D. F., Venkatesh, S., Parikh, D., Maira, A., Srinivasan, A., Zheng, W., Tarabra, E., Zong, H., Jayakumar, S., Jeganathan, V., Pradan, K., Aleman, J. O., Singh, R., Nandi, S., Pessin, J. E., & Sibinga, N. E. S. (2023). Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1. Nature communications, 14(1), Article 38. https://doi.org/10.1038/s41467-022-35683-7

Chinnasamy, P, Casimiro, I, Riascos-Bernal, DF, Venkatesh, S, Parikh, D, Maira, A, Srinivasan, A, Zheng, W, Tarabra, E, Zong, H, Jayakumar, S, Jeganathan, V, Pradan, K, Aleman, JO, Singh, R, Nandi, S, Pessin, JE & Sibinga, NES 2023, 'Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1', Nature communications, vol. 14, no. 1, 38. https://doi.org/10.1038/s41467-022-35683-7

@article{61ad094ddfa2470aa16cf9f344fc3d70,

title = "Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1",

abstract = "Recent studies implicate macrophages in regulation of thermogenic, sympathetic neuron-mediated norepinephrine (NE) signaling in adipose tissues, but understanding of such non-classical macrophage activities is incomplete. Here we show that male mice lacking the allograft inflammatory factor-1 (AIF1) protein resist high fat diet (HFD)-induced obesity and hyperglycemia. We link this phenotype to higher adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance by AIF1-deficient macrophages, and find through reciprocal bone marrow transplantation that donor Aif1-/- vs WT genotype confers the obesity phenotype in mice. Interestingly, human sequence variants near the AIF1 locus associate with obesity and diabetes; in adipose samples from participants with obesity, we observe direct correlation of AIF1 and MAOA transcript levels. These findings identify AIF1 as a regulator of MAOA expression in macrophages and catecholamine activity in adipose tissues – limiting energy expenditure and promoting energy storage – and suggest how it might contribute to human obesity.",

author = "Prameladevi Chinnasamy and Isabel Casimiro and Riascos-Bernal, {Dario F.} and Shreeganesh Venkatesh and Dippal Parikh and Alishba Maira and Aparna Srinivasan and Wei Zheng and Elena Tarabra and Haihong Zong and Smitha Jayakumar and Venkatesh Jeganathan and Kith Pradan and Aleman, {Jose O.} and Rajat Singh and Sayan Nandi and Pessin, {Jeffrey E.} and Sibinga, {Nicholas E.S.}",

note = "Publisher Copyright: {\textcopyright} 2023, The Author(s).",

year = "2023",

month = dec,

doi = "10.1038/s41467-022-35683-7",

language = "English (US)",

volume = "14",

journal = "Nature communications",

issn = "2041-1723",

publisher = "Nature Publishing Group",

number = "1",

}

TY - JOUR

T1 - Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1

AU - Chinnasamy, Prameladevi

AU - Casimiro, Isabel

AU - Riascos-Bernal, Dario F.

AU - Venkatesh, Shreeganesh

AU - Parikh, Dippal

AU - Maira, Alishba

AU - Srinivasan, Aparna

AU - Zheng, Wei

AU - Tarabra, Elena

AU - Zong, Haihong

AU - Jayakumar, Smitha

AU - Jeganathan, Venkatesh

AU - Pradan, Kith

AU - Aleman, Jose O.

AU - Singh, Rajat

AU - Nandi, Sayan

AU - Pessin, Jeffrey E.

AU - Sibinga, Nicholas E.S.

PY - 2023/12

Y1 - 2023/12

N2 - Recent studies implicate macrophages in regulation of thermogenic, sympathetic neuron-mediated norepinephrine (NE) signaling in adipose tissues, but understanding of such non-classical macrophage activities is incomplete. Here we show that male mice lacking the allograft inflammatory factor-1 (AIF1) protein resist high fat diet (HFD)-induced obesity and hyperglycemia. We link this phenotype to higher adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance by AIF1-deficient macrophages, and find through reciprocal bone marrow transplantation that donor Aif1-/- vs WT genotype confers the obesity phenotype in mice. Interestingly, human sequence variants near the AIF1 locus associate with obesity and diabetes; in adipose samples from participants with obesity, we observe direct correlation of AIF1 and MAOA transcript levels. These findings identify AIF1 as a regulator of MAOA expression in macrophages and catecholamine activity in adipose tissues – limiting energy expenditure and promoting energy storage – and suggest how it might contribute to human obesity.

AB - Recent studies implicate macrophages in regulation of thermogenic, sympathetic neuron-mediated norepinephrine (NE) signaling in adipose tissues, but understanding of such non-classical macrophage activities is incomplete. Here we show that male mice lacking the allograft inflammatory factor-1 (AIF1) protein resist high fat diet (HFD)-induced obesity and hyperglycemia. We link this phenotype to higher adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance by AIF1-deficient macrophages, and find through reciprocal bone marrow transplantation that donor Aif1-/- vs WT genotype confers the obesity phenotype in mice. Interestingly, human sequence variants near the AIF1 locus associate with obesity and diabetes; in adipose samples from participants with obesity, we observe direct correlation of AIF1 and MAOA transcript levels. These findings identify AIF1 as a regulator of MAOA expression in macrophages and catecholamine activity in adipose tissues – limiting energy expenditure and promoting energy storage – and suggest how it might contribute to human obesity.

UR - http://www.scopus.com/inward/record.url?scp=85145428387&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85145428387&partnerID=8YFLogxK

U2 - 10.1038/s41467-022-35683-7

DO - 10.1038/s41467-022-35683-7

M3 - Article

C2 - 36596796

AN - SCOPUS:85145428387

SN - 2041-1723

VL - 14

JO - Nature communications

JF - Nature communications

IS - 1

M1 - 38

ER -

Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this