Suneil Koliwad, MD, PhD

Associate Professor
Diabetes Center
Research Overview: 

My laboratory investigates the role of chronic inflammation in the development of Type 2 Diabetes and how dietary lipids modulate the activation of innate immune cells that trigger and maintain inflammation in metabolic tissues.

Beyond comprising our bodily energy stores, dietary lipids are necessary for several critical processes, including the synthesis of cellular membranes, vitamins, skin lipids and waxes, blood clotting, gene expression, and cell signaling cascades. However, when chronically in excess, dietary fat intake is associated with several diseases, including diabetes, neurodegenerative diseases, certain cancers, and atherosclerosis, which together exact a huge toll on human health. Given the high prevalence of high-fat diets in our world, determining the links between dietary lipids and these diseases is of biomedical and socioeconomic importance. 

One emerging possibility involves chronic inflammation. Excess dietary fat intake often produces tissue inflammation that manifests prior to disease onset. For type 2 diabetes, this process is characterized by the inflammatory (M1) activation of innate immune cells, including macrophages and dendritic cells, in metabolic tissues such as white adipose, muscle, and liver. In exploring how dietary lipids may act as proximal triggers of macrophage activation, we showed that genetically-altered murine macrophages with an increased capacity to store dietary fats as intracellular triacylglycerol are less vulnerable to M1 inflammatory activation both in culture and in living mice. Remarkably, by transplanting these protective macrophages into mice protected them against developing diabetes driven by diet-induced obesity.

We are now deeply focused on probing the mechanisms by which intracellular fatty acids modulate inflammatory activation in macrophages, dendritic cells, and CNS microglia and determine how these impact type 2 diabetes, neurodegeneration, and other diseases in which chronic inflammation precedes overt disease.

Primary Thematic Area: 
Tissue / Organ Biology & Endocrinology
Secondary Thematic Area: 
Research Summary: 
The Intersection between Dietary Lipids, Inflammation, and Metabolic Disease



Blocking Kv1.3 potassium channels psrevents postoperative neuroinflammation and cognitive decline without impairing wound healing in mice.

British journal of anaesthesia

Lai LK, Valdearcos M, Morioka K, Saxena S, Feng X, Li R, Uchida Y, Lijun A, Li W, Pan J, Koliwad S, Marcucio R, Wulff H, Maze M

CD81 Controls Beige Fat Progenitor Cell Growth and Energy Balance via FAK Signaling.


Oguri Y, Shinoda K, Kim H, Alba DL, Bolus WR, Wang Q, Brown Z, Pradhan RN, Tajima K, Yoneshiro T, Ikeda K, Chen Y, Cheang RT, Tsujino K, Kim CR, Greiner VJ, Datta R, Yang CD, Atabai K, McManus MT, Koliwad SK, Spiegelman BM, Kajimura S

1769-P: Microglial Activation and Inactivation via Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) Alters Peripheral Glucose Homeostasis.



Neuronal modulation of hepatic lipid accumulation induced by binge-like drinking.

American journal of physiology. Endocrinology and metabolism

Ibars M, Maier MT, Yulyaningsih E, Perez L, Cheang R, Vilhelmsson A, Louie SM, Wegner SA, Yuan X, Eltzschig HK, Hopf FW, Nomura DK, Koliwad SK, Xu AW