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From the Hospital of the University of Pennsylvania and Philadelphia Veterans Affairs Medical Center, Philadelphia, Pennsylvania.
Note: Dr. Iqbal is currently an adjunct faculty member at the University of Pennsylvania and is employed at Bristol-Myers Squibb, Lawrenceville, New Jersey.
Acknowledgment: The authors thank Thomas A. Wadden, PhD, for his critical review of the manuscript and James P. Guevara, MD, MPH, for his expertise in qualitative assessment.
Potential Financial Conflicts of Interest:Employment: N. Iqbal (Bristol-Myers Squibb).
Requests for Single Reprints: Marion L. Vetter, MD, RD, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Hospital of the University of Pennsylvania, One Maloney Building, 3400 Spruce Street, Philadelphia, PA 19104; e-mail, email@example.com.
Current Author Addresses: Drs. Vetter, Cardillo, Rickels, and Iqbal: Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Hospital of the University of Pennsylvania, One Maloney Building, 3400 Spruce Street, Philadelphia, PA 19104.
Bariatric surgery leads to substantial and durable weight reduction. Nearly 30% of patients who undergo bariatric surgery have type 2 diabetes, and for many of them, diabetes resolves after surgery (84% to 98% for bypass procedures and 48% to 68% for restrictive procedures). Glycemic control improves in part because of caloric restriction but also because gut peptide secretion changes. Gut peptides, which mediate the enteroinsular axis, include the incretins glucagon-like peptide-1 and glucose-dependent insulinotropic peptide, as well as ghrelin and peptide YY. Bariatric surgery (particularly bypass procedures) alters secretion of these gut hormones, which results in enhanced insulin secretion and sensitivity. This review discusses the various bariatric procedures and how they alter the enteroinsular axis. Familiarity with these effects can help physicians decide among the different surgical procedures and avoid postoperative hypoglycemia.
Reprinted with permission of the American Society for Metabolic and Bariatric Surgery, copyright 2008, all rights reserved.
The relationship is best described by a hyperbolic function, so that any change in insulin sensitivity is balanced by a reciprocal and proportionate change in insulin secretion. Glucose tolerance is determined by the interaction of insulin secretion and sensitivity, so that patients with normal glucose tolerance are at about the 50th percentile and those below it exhibit increasing impairment to diabetic glucose tolerance. Reproduced from reference 84, with permission of the American Diabetes Association.
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