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 and Nicholas E. S. Sibinga ()
Additional contact information
Prameladevi Chinnasamy: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Isabel Casimiro: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Dario F. Riascos-Bernal: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Shreeganesh Venkatesh: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Dippal Parikh: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Alishba Maira: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Aparna Srinivasan: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Wei Zheng: Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
Elena Tarabra: Department of Molecular Pharmacology, Albert Einstein College of Medicine
Haihong Zong: Department of Medicine (Endocrinology, Albert Einstein College of Medicine)
Smitha Jayakumar: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Venkatesh Jeganathan: Department of Medicine (Cardiology), Albert Einstein College of Medicine
Kith Pradan: Albert Einstein College of Medicine
Jose O. Aleman: New York University Langone Health
Rajat Singh: Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
Sayan Nandi: Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
Jeffrey E. Pessin: Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine
Nicholas E. S. Sibinga: Department of Medicine (Cardiology), Albert Einstein College of Medicine

Nature Communications, 2023, vol. 14, issue 1, 1-13

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41467-022-35683-7

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