Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery.

Publication Date: 2010 Feb 2 PMID: 20133150
Authors: Karra, E. - Yousseif, A. - Batterham, R. L.
Journal: Trends Endocrinol Metab

Bariatric surgery is the most effective treatment modality for obesity, resulting in durable weight loss and amelioration of obesity-associated comorbidities, particularly type 2 diabetes mellitus (T2DM). Moreover, the metabolic benefits of bariatric surgery occur independently of weight loss. There is increasing evidence that surgically induced alterations in circulating gut hormones mediate these beneficial effects of bariatric surgery. Here, we summarise current knowledge on the effects of different bariatric procedures on circulating gut hormone levels. We also discuss the theories that have been put forward to explain the weight loss and T2DM resolution following bariatric surgery. Understanding the mechanisms mediating these beneficial outcomes of bariatric surgery could result in new non-surgical treatment strategies for obesity and T2DM.

post to: CiteULike

New study finds possible source of beta cell destruction that leads to Type 1 diabetes

Doctors at Eastern Virginia Medical School's Strelitz Diabetes Center have been stalking the culprit responsible for Type 1 diabetes. Now, they are one step closer. (2010-02-05)

ROLE OF MELANOCORTIN RECEPTOR ACCESSORY PROTEINS IN THE FUNCTION OF ZEBRAFISH MELANOCORTIN RECEPTOR TYPE 2

Genetic Determinants of Pubertal Timing in the General Population

Inhibitory effect of pituitary adenylate cyclase activating polypeptide on the initial stages of rat follicle development

Mitochondrial dysfunction is induced by high levels of glucose and free fatty acids in 3T3-L1 adipocytes

GENETICS AND PHENOMICS OF INHERITED AND SPORADIC NON-AUTOIMMUNE HYPERTHYROIDISM

Progesterone Inhibits Apoptosis in part by PGRMC1-Regulated Gene Expression

TGF-beta induces telomerase-dependent pancreatic tumor cell cycle arrest

ESTRIOL ACTS AS A GPR30 ANTAGONIST IN ESTROGEN RECEPTOR-NEGATIVE BREAST CANCER CELLS