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Role of microglial cGAS in metabolic regulation

Award Number: F32DK149478
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/30/2026
PERIOD OF PERFORMANCE END DATE: 09/29/2027

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Role of microglial cGAS in metabolic regulation - PROJECT SUMMARY Obesity is a major global health challenge associated with type 2 diabetes, cardiovascular disease, and reduced quality of life. Although hypothalamic neurons that regulate feeding and energy expenditure have been extensively studied, the non-neuronal cells that shape these circuits, particularly microglia, remain underexplored. Microglia rapidly respond to nutritional states. For example, high-fat diet triggers pro-inflammatory activation that impairs hypothalamic circuits and drives diet-induced obesity, whereas fasting promotes anti-inflammatory remodeling that supports adaptive metabolic responses. However, the molecular mechanisms through which microglia sense dynamic dietary cues and alter whole-body metabolism are poorly defined. Single-nucleus RNA- seq data from my preliminary work revealed that the DNA sensor cyclic GMP–AMP synthase (cGAS) in arcuate nucleus (ARH) microglia is strongly regulated by nutritional status, which is upregulated during fasting and downregulated by HFD. Strikingly, microglia-specific deletion of Cgas causes significant weight loss in chow-fed mice independent of food intake, revealing an unexpected role for cGAS in energy homeostasis. Yet how dietary signals regulate microglial cGAS, and how cGAS in turn influences neuronal circuits and metabolism, remain unknown. This proposal aims to define the physiological and mechanistic roles of microglial cGAS in metabolic adaptation. Aim 1 will determine how microglial cGAS regulates whole-body energy balance during fasting, refeeding, and HFD challenge through assessments of energy expenditure, counterregulatory glucose responses, and food-seeking behavior. Aim 2 will define the upstream triggers and downstream pathways of microglial cGAS during diet-induced metabolic adaptation by mapping cGAS and DNA subcellular localization, assessing STING-dependent and -independent pathways, and evaluating microglial functions. These studies will uncover a previously unrecognized metabolic function of microglial cGAS, establishing how nutritional cues interface with neuroimmune signaling to shape energy homeostasis. The proposed work leverages my background in mouse metabolism and provides rigorous training in microglial biology, neural circuitry, and advanced imaging, supporting my development into an independent scientist studying neural regulation of metabolism.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $76,780 )
2026	2026	UNIVERSITY OF SOUTH FLORIDA	4202 E FOWLER AVE	TAMPA	FL	33620	HILLSBOROUGH	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	8/3/2026	NEW	$76,780
														Subtotal = $76,780

Grand Total All Awards = $76,780

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Role of microglial cGAS in metabolic regulation

Award Number: F32DK149478

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/30/2026

PERIOD OF PERFORMANCE END DATE: 09/29/2027

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