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Editorial Obesity and Weight Management The Birth of Bariatric Endocrinology and the Coming of Age of Obesity Medicine J Michael Gonzalez-Campoy Minnesota Center for Obesity, Metabolism and Endocrinology, Eagan, US Abstract The number of publications about obesity has increased geometrically over the past couple of decades. The knowledge that adipose tissue is an endocrine organ gave birth to the field of bariatric endocrinology. The concept that adipose tissue may become diseased, and thus contribute to the genesis of metabolic disorders, including hyperglycemia, dyslipidemia, hypertension, male hypogonadism, and cardiovascular disease, constitutes adiposopathy. The goals of treatment for people with overweight and obesity are to decrease the burden of fat mass (adiposity), and to treat adiposopathy (i.e. to return adipose tissue function to normal). As a society, we must overcome the social, political and economic obstacles that prevent patients with overweight or obesity from gaining access to needed medical care. Keywords Bariatric endocrinology, obesity, adiposopathy, vagal blockade, intra-gastric balloon, weight loss medications, bariatric surgery Disclosure: J Michael Gonzalez-Campoy has received speaker honoraria from Amylin, Astra Zeneca, Vivus, Eisai, Janssen, GSK, Takeda, Novo Nordisk and Shire. He has received research grants from Sanofi-Aventis, Novo Nordisk, Astra-Zeneca, Boehringer Ingelheim, Ipsen, Eli Lilly, Bristol Myers Squibb and Mannkind. He is a consultant for ValenTx, Corcept and Novo Nordisk. This article is a short opinion piece and has not been submitted to external peer reviewers. No funding was received in the publication of this article. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, adaptation, and reproduction provided the original author(s) and source are given appropriate credit. Received: April 5, 2016 Published Online: April 15, 2016 Citation: US Endocrinology 2016;12(1):10–1 Correspondence: J Michael Gonzalez-Campoy, Minnesota Center for Obesity, Metabolism and Endocrinology, PA (MNCOME), 1185 Town Centre Drive, Suite 220, Eagan, MN 55123, US. E: drmike@mncome.com A search of PubMed shows that in 1960, the year I was born, there were 110 publications on obesity. In 1991, the year I graduated from Mayo Medical School, the number had risen to 406 publications. By contrast, in 2015 there were 5470 publications on obesity. The last quarter of a century has led to the recognition of a world-wide epidemic of overweight and obesity, with a rise in all their complications. 1–3 And with this recognition came the need to understand the underlying physiology and pathophysiology, and the eventual development of therapeutic interventions. 4–6 It is now clear that the accretion of adipose tissue (adiposity) leads to physical complications (i.e. sleep apnea, gastroesophageal reflux disease, degenerative osteoarthritis, and dermopathy). It is also universally recognized that adipose tissue is not just an energy storage organ. Rather, adipose tissue is an endocrine organ which actively makes and responds to hormones. As such, adipose tissue is a major contributor to energy homeostasis. An emerging concept is that derangements of adipose tissue function contribute to the genesis of metabolic diseases (i.e. diabetes, hypertension, dyslipidemia, cardiovascular disease). My colleague, Harold Bays, introduced the concept of adiposopathy (sick fat) into the medical literature. 7,8 Adiposopathy defines the anatomic and functional changes that lead to adipose tissue dysfunction, and thus contribute to metabolic diseases. 10 Adiposopathy is anatomically manifested by adipocyte hypertrophy, visceral adiposity (best measured by the waist circumference), growth of adipose tissue beyond its vascular supply, increased number of adipose tissue immune cells, and ectopic fat deposition (in other body organs). Functionally, adiposopathy is manifested by impaired adipogenesis, heterogeneous distribution of adipose tissue (i.e. preferential accumulation of intra-abdominal, visceral fat), adipocyte lipolysis in excess of lipogenesis, increased free fatty acids, pathogenic adipose tissue endocrine responses (i.e. hypoadiponectinemia and hyperleptinemia), pathogenic adipose tissue immune responses, and pathogenic crosstalk between adipose tissue and other organs. 8–11 Bariatric endocrinology was born from the need to address adipose tissue as an endocrine organ, and to study the role of adiposopathy in the etiology of metabolic diseases. Further, bariatric endocrinology focuses on the development of medical interventions that return adipose tissue normal. Whereas the loss of adipose tissue mass improves the complications of adiposity, the treatment of adiposopathy, independent of fat mass, is now a primary treatment target. 12 Surrogate measures of adipose tissue function, including insulin resistance, increased waist circumference, hypertriglyceridemia and low levels of the high density lipoprotein cholesterol (the elements of the dysmetabolic TOUCH ME D ICA L ME D IA