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        Postprandial Hypoglycemia in Polycystic Ovarian Syndrome and Pancreatic Beta Cell Response: Presented at ENDO

          By Louise Gagnon

          TORONTO, CANADA -- June 7, 2007 -- Women with polycystic ovary syndrome who experience postprandial hypoglycemia may have an altered pancreatic beta-cell response, researchers have postulated in a study.

          In a poster presentation here at the 89th annual meeting of the Endocrine Society (ENDO), investigators presented data from a small study of women with PCOS, demonstrating the prevalence of hypoglycemia in the sample.

          Sharan Gill, MD, first-year clinical fellow, endocrinology, University of California, Davis, Sacramento, California, United States, noted that her colleagues published research in the American Journal of Clinical Nutrition (2007;85(3):688-694) showing PCOS patients had significant postprandial hypoglycemia, which activated cortisol and adrenal androgen secretion when glucose levels dropped below 69 mg/dl during the oral glucose tolerance test (OGTT).

          In this study, Dr. Gill and colleagues recruited 36 patients with PCOS in the community who underwent a five-hour, 75g-OGTT. In addition, they underwent a three-hour frequent sample intravenous glucose tolerance test (FS-IVGTT), assessed using the minimal model.

          A total of 21 patients with a plasma glucose nadir of 64.0 mg/dl were categorized as hypoglycemic (58%) while the balance of patients who had a plasma glucose nadir of 77.0 mg/dl was categorized as non-hypoglycemic.

          "We would not have thought that they experience post-prandial hypoglycemia," said Dr. Gill. "Patients who were hypoglycemic were found to have decreased serum glucose, decreased insulin, and decreased homeostatic model assessment, compared to non-hypoglycemic patients: 99.5 vs. 101.7 mg/dl, 18.3 vs. 22.2 mUL-1, and 5.2 vs. 6.2, respectively.

          Another observation that researchers noted was the elevation in insulin during the first 90 minutes of the OGTT: area under the curve insulin 316 vs. 260 mU/ml. Hypoglycemic patients experienced an elevation in serum cortisol between three hours and four hours, increasing from 5.6 mcg/dl to 12.2 mcg/dl. In contrast, non-hypoglycemic patients did not experience a rise in cortisol levels in the same time period, 8.9 mcg/dl to 7.6 mcg/dl.

          Moreover, the hypoglycemic patients had increased acute insulin secretory response to glucose (AIRg 737 vs. 371mUL-1 min-1) during FS-IVGTT while insulin sensitivity between hypoglycemic and non-hypoglycemic subjects was comparable: 4.2 vs. 4.1 mU/L-1min-1.

          "It appears in the hypoglycemic patients that the pancreas is working overtime and secreting more insulin initially to cause hypoglycemia later on," said Dr. Gill, stressing that insulin sensitivity was the same between hypoglycemic and non-hypoglycemic patients.

          "We think this reflects the beta-cell function in the pancreas, that it is secreting more insulin than required," said Dr. Gill.

          Dr. Gill suggested that PCOS patients do not intake large amounts of carbohydrates at mealtime to avoid the potential development of hypoglycemia and associated symptoms after eating. "If they have a large meal that is heavy in carbohydrates, they may have symptoms like tremors and shakes," said Dr. Gill.

          The U.S. National Institutes of Health funded the study.


          [Presentation title: Postprandial Hypoglycemia in Polycystic Ovarian Syndrome (PCOS) Is Related to Pancreatic Beta Cell Response. Abstract P4-201]




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