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The contents of the proximal jejunum and distal ileum were cultured quantitatively in eight patients who were undergoing intestinal bypass procedure for obesity. Five jejunal specimens were sterile, and three contained low counts of a predominantly aerobic flora. Ileal contents yielded variable but usually higher counts than in the jejunum, and there were similar numbers of anaerobes and aerobes. In three patients in whom a bypass was established, contents of the functioning small bowel showed counts of 10(5.0)-10(7.6) colony-forming units/ml. These counts exceeded the counts in the normal terminal ileum, and the flora qualitatively resembled that of feces. Four specimens from excluded loops revealed colonization with fecal organisms, and the counts ranged between 10(6.4) and 10(9.7) colony-forming units/ml. In jejunoileal bypass both the functioning small bowel and the excluded loop become colonized with colonic flora, a phenomenon that may contribute to some of the side effects of this procedure.

This study was carried out to determine if, in fasting, an adaptation to utilization of ketones could prevent cerebral dysfunction during periods of acute, insulin-induced glucopenia. In the course of standard insulin tolerance tests (0.1-0.2 U/kg), nine obese subjects manifested frank hypoglycemic reactions resulting in an increase in urinary catecholamine excretion from 61 to 113 mug/24 hr (P < 0.01). After fasting 2 months, administration of weight-adjusted doses of insulin produced identical maximum insulin concentrations and disappearance curves. However, no insulin reactions nor significant rises in catecholamine excretion occurred despite equal extent and rate of glucose fall. Glucose concentrations as low as 0.5 mmoles/liter (9 mg/100 ml) failed to precipitate hypoglycemic reactions. During the postfast insulin tolerance tests, mean plasma 2-hydroxybutyrate (beta-OHB) decreased from 8.02 to 6.69 mmoles/liter (P < 0.01). In another five fasting subjects tested, the A-V difference for beta-OHB across brain increased progressively from 0.21 to 0.70 mmoles/liter whereas across the forearm no consistent uptake could be demonstrated. Simultaneously, the A-V difference across the brain for glucose decreased from 0.24 to 0.07 mmoles/liter of plasma. In addition to insulin-induced suppression of hepatic ketogenesis, the augmented cerebral ketone uptake during insulin hypoglycemia contributes to the net fall in plasma beta-OHB. Ketoacids, extracted by the fast-adapted brain, supplant glucose as a metabolic substrate preventing overt hypoglycemic reactions during acute glucopenia.