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Pelvic lipomatosis is a disease of dense infiltration of benign fatty tissue within the confines of the deep bony pelvis. A case is reported of an obese, hypertensive, thirty-nine-year-old black man with the typical clinical and radiographic features of pelvic lipomatosis. Prolonged fasting produced an extensive weight loss and profound resolution of his presenting symptoms, signs, and radiologic abnormalities. Subsequent regain of weight resulted in the reappearance of the disorder, confirming that pelvic lipomatosis may be a disease of accelerated and excessive fat deposition which can be reversed by dietary restriction. The literature pertaining to pelvic lipomatosis is reviewed in detail.

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.