Previous studies by the authors have suggested an increased plasma beta-endorphin response to glucose ingestion in obese subjects compared with controls. The present study confirms these earlier findings and demonstrates a parallel increase in plasma ACTH in obese subjects compared with normal-weight controls. It seems likely that this response is the result of increased production of beta-endorphin by the pituitary. Suggestions for further research are made.
Studies of the effects of opiate antagonists in humans indicate that central opiates are probably involved in the control of eating in both obese and lean subjects. Naloxone, an opiate antagonist which crosses the blood-brain barrier, decreased eating in obese humans but not in lean controls . These data led to the suggestion that endogenous opiates might play a role in control of food intake in obese, but not in lean, humans. However, long-term administration of naltrexone, a long-acting opiate antagonist, did not produce weight loss in obese humans (Malcolm, O'Neil, Sexauer, Riddle, Currey, & Counts, 1985). Furthermore, two groups of investigators have reported that lean subjects as well as obese humans eat less following single doses of naloxone (Trenchard & Silverstone, 1983; Cohen, Cohen, Pickar, & Murphy, 1985). Naloxone also blocked eating, but not hunger, induced by 2-deoxy-D-glucose, in a group of normal-weight subjects (Thompson, Welle, Lilavivat, Penicaud,