There is a pressing need for new therapeutic strategies to address the epidemic of obesity and its co-morbidities. Bariatric surgery, a surgical manipulation of the gut for weight loss, causes remarkable improvements in obesity and several of its co-morbidities. Specifically, bariatric surgery causes remission of type 2 diabetes (T2DM) and cardiovascular diseases (CVD) such as hypertension. Bariatric surgery also substantially decreases the risk of cancer. Importantly, the metabolic benefits of bariatric surgery often occur prior to weight loss, suggesting that mechanisms other than body weight contribute. Identification of the mechanisms underlying these surgically-induced benefits will provide insight into the basic biology by which the gut regulates whole body physiology, leading to the development of novel therapies for managing obesity and its co-morbidities. Thus, the overall theme of our research program is identifying the mechanisms by which bariatric surgery causes these health benefits using animal models of bariatric surgery. The primary mechanisms of interest in our lab are glucagon-like peptide-1 (GLP-1) and bile acid signaling.

GLP-1 is a hormone secreted by gastrointestinal enteroendocrine cells in response to nutrient ingestion. GLP-1 contributes to postprandial glucose clearance by potentiating glucose-stimulated insulin secretion. GLP-1 signaling also promotes several other metabolic benefits, including decreased energy intake, improved insulin sensitivity and improved lipid metabolism. Therefore, GLP-1 has become an important therapeutic target in the clinical management of obesity and type 2 diabetes. Nutrient-stimulated GLP-1 secretion is remarkably enhanced after bariatric surgery. We have published work showing that GLP-1 signaling improves glucose regulation by enhancing islet function after bariatric surgery. Therefore, current work in our lab is investigating how GLP-1 receptor signaling improves islet function after bariatric surgery using various genetically modified mouse models.

Circulating bile acid concentrations are elevated after bariatric surgery. Bile acids are amphipathic steroid molecules with detergent properties that aid in the digestion of dietary cholesterol and lipid. Bile acids also contribute to glucose homeostasis by signaling through several receptors, including TGR5. We have published work showing that TGR5 contributes to improved glucose regulation after bariatric surgery. This work also identified a novel role for TGR5 in the regulation of bile acid metabolism which has implications on treatment strategies for diabetes, cardiovascular disease and cancer. Therefore, we have ongoing studies in various genetically and pharmaceutically modified mouse models investigating how TGR5 contributes to the effect of bariatric surgery to improve these obesity co-morbidities.

06/2011   DVM, University of California, Davis                                  
12/2009   PhD (Physiology), University of California, Davis                        
05/2005   BS Biology (High Honors), Brandeis University, Waltham, MA 
05/2005   BA Economics, Brandeis University, Waltham, MA

09/2013-present  Assistant Professor, Cornell University, Dept. of Biomedical Sciences, CVM
03/2013-08/2013 Assistant Adjunct Professor, UC Davis, Dept. of Molecular Biosciences, SVM
08/2011-02/2013 Assistant Project Biochemist, UC Davis, Dept. of Molecular Biosciences, SVM
12/2009-07/2011 Post-Doctoral Fellow, UC Davis, Dept. of Nutrition

1. McGavigan AK, Henseler Z, Garibay D, Butler SD, Jayasinghe S, Ley RE, Davisson RL, Cummings BP. Vertical sleeve gastrectomy surgery reduces arterial blood pressure and hypothalamic endoplasmic reticulum stress in mice. DMM, in press.
2. Garibay D, McGavigan AK, Lee SA, Ficorilli JV, Cox AL, Michael MD, Sloop KW, Cummings BP. Beta-cell glucagon like peptide-1 receptor contributes to improved glucose tolerance after vertical sleeve gastrectomy. Endocrinology. 2016; 157:3405-9.
3. McGavigan AK, Garibay D,  Henseler Z, Chen J, Bettaieb A, Haj FG, Ley RE, Chouinard ML, Cummings BP. TGR5 contributes to glucoregulatory improvements after sleeve gastrectomy in mice. Gut. 2015; 0:1-9.
4. Mann S, Leal Yepes FA, Duplessis M, Wakshlag JJ, Overton TR, Cummings BP, Nydam DV. Dry period plane of energy: effects on glucose tolerance in transition dairy cows. Journal of Dairy Science. In press.
5. Frank L, Mann S, Levine CB, Cummings BP, Wakshlag JJ. Increasing body condition score is positively associated interleukin-6 and monocyte chemoattractant protein-1 in Labrador retrievers. Vet Immunol Immunopathol. 2015; 167(3-4):104-9.
6. von Pfeil DF, Cummings BP, Loftus JP, Levine CB, Sabine Mann, Downey RL, Griffitts C, Wakshlag JJ. Evaluation of Plasma Inflammatory Myokine Concentrations in Racing Sled Dogs. Canadian Veterinary Journal. In press.
7. Streeter RM, Struble AM, Nydam DV, Bauer JE, Castellano M, Todhunter RJ, Cummings BP, Wakshlag JJ. The associations between serum adiponectin, leptin, c-reactive protein and insulin and serum long-chain omega three fatty acids in Labrador retrievers. Veterinary Medicine: Research and Reports. 2015; 6:103-110.
8. Bu P, Wang L, Chen K, Rakhilin N, Sun J, Closa A, Tung K, King S, Varanko AK, Yitian Xu Y, Chen JH, Zessin AS, Shealy J, Cummings BP, Hsu D, Lipkin SM, Moreno V, Gümüş ZH, Shen X. miR-1269 Promotes Metastasis and Forms a Positive Feedback Loop with TGF-β. Nat Communications. 2015; 6:6879.
9. Alley JB, Laferrere B, Cummings BP. A road to remission: Multiple perspectives – Bariatric surgery and its effect on metabolic disease. Endocrine News: Tri-Point Series. Endocrine News: Tri-Point Series: 26-30, April 2015.
10. Cummings BP. Duodenal exclusion devices: promising tools in treating obesity and type 2 diabetes. Gut. 2014; 63(8):1201-2.

Browse PubMed for a complete listing of Dr. Cummings's publications

• 2019 Schwartz Research Fund Awardee
• 2019 Hartwell Individual Biomedical Research Awardee
• 2014 Burroughs Welcome Fund Becoming Faculty Workshop Invitee
• 2011 Dr. Wild Fellowship Award for excellence in research
• 2010 Dr. Max Kleiber Award for a distinguished doctoral thesis
• 2009 Dr. Charles E. Cornelius Memorial Fellowship for excellence in research
• 2008 Dr. Richard A. Freedland Fellowship Award for excellence in research
• 2007-2008 NIH T35 YEAR Fellowship
• 2007-2009 NIH T32 STAR Fellowship
• 2006 Achievement Rewards for College Scientists Fellowship
• 2005-2011 Veterinary Scientist Training Program Fellowship
• 2004 Howard Hughes Medical Institute Summer Fellowship

• Comparative Biomedical Sciences
• Molecular and Integrative Physiology
• Graduate Field of Nutrition