Gut Hormones, Obesity, Polycystic Ovarian Syndrome, Malignancy, and Lipodystrophy Syndromes
- Zachary T. Bloomgarden, MD, is a practicing endocrinologist in New York, New York, and is affiliated with the Division of Endocrinology, Mount Sinai School of Medicine, New York, New York
- CVD, cardiovascular disease
- FFA, free fatty acid
- GLP, glucagon-like peptide
- GnRH, gonadotropin releasing hormone
- IGF, insulin-like growth factor
- IGT, impaired glucose tolerance
- IRS, insulin resistance syndrome
- NPY, neuropeptide-Y
- OXM, oxyntomodulin
- PCOS, polycystic ovary syndrome
- PPAR, peroxisome proliferator–activator receptor
- PYY, peptide YY
- RGZ, rosiglitazone
- SSPG, steady-state plasma glucose
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This is the third in a series of four articles on presentations at the World Congress on the insulin resistance syndrome (IRS), reviewing relationships between insulin resistance and gut hormones, obesity, polycystic ovarian syndrome, malignancy, and lipodystrophy syndromes.
Gut hormones
Steve Bloom (London, U.K.) discussed satiety signals, noting that obesity is “key to the [insulin resistance] syndrome” and that it ultimately is caused by overeating. Childhood obesity is on the rise, with 40% of children expected to be overweight by 2010. He asked, what explains the reduction in hunger after a meal? Bulk in the stomach and nutrients in the circulation appear not to be the cause. There must be specific signals from the gut to the brain, neural and/or hormonal. It appears that, when stimulated, a small area in the proximal gastric fundus, near the esophagus, sends vagal signals mediating satiety. Studies have attempted to replicate gut hormonal signals by infusion, with cholecystokinin (CCK) decreasing food intake but causing pancreatitis and acting as a growth factor for pancreatic acinar cells, which could cause increased pancreatic cancer risk. Ghrelin decreases after meals and may be a negative satiety signal, as its direct effect is to stimulate food intake. Pancreatic polypeptide may be a factor, and the distal small bowel and colon produce glucagon-like peptide (GLP)-1, oxyntomodulin, and peptide YY (PYY), additional candidate …
