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A B S T R A C T Lipolytic activity was studied in esophageal and gastric aspirates obtained with a nasogastric tube from 14 healthy adult subjects. Samples were collected from esophagus, first at 30-35 cm and then at 40-45 cm from the nose, as the subject, after drinking 15-30 ml of a cream-milk mixture, swallowed small amounts of water. The samples from stomach were taken last and usually contained a small amount of cream-milk mixture. Lipolytic activity was assayed using chylomicron, milk, and corn oil triglyceride as substrate. Esophageal and gastric samples both contained lipolytic activity which hydrolyzed long-chain triglyceride to diglyceride, monoglyceride, and FFA, had a pH optimum of 5.4, and was not affected by either 0.5 M NaCl or 4 mM sodium taurodeoxycholate. The activity, expressed as nanomoles of chylomicron triglyceride hydrolyzed per milliliter per minute, ranged from 0 to 145 in upper esophageal, 5 to 303 in lower esophageal, and 50 to 357 in gastric samples. Only a trace of lipolytic activity was found at pH 5.4 in saliva collected from the parotid, submandibular, and sublingual glands, thus excluding those tissues as a source of the activity found in esophageal and gastric aspirates. The findings suggest that in man glands in or near the pharynx secrete a lipase that acts in the stomach to hydrolyze long-chain triglyceride to partial glycerides and FFA. It is proposed that this reaction is the first step in the digestion of dietary fat and that the amphi-

Pregnant rats fasted on the 18th or 19th day of gestation developed hypoglycemia, severe ketosis, and hyperlipemia. The latter, which consisted primarily of triglycerides, was accompanied by increased plasma free fatty acids and accumulation of fat in the liver and kidneys. The effects of fasting were diminished by starting the fast earlier in pregnancy or by hysterectomy. Both ketosis and hyperlipemia were corrected by administration of insulin, tolbutamide, or glucose. The findings indicate that increased fat mobilization and ketosis in fasting pregnant rats are the result of insulin lack. It is suggested that the high priority of the fetuses for glucose reduced the maternal blood glucose concentration to a level too low to stimulate insulin secretion during fasting. Fasting did not alter the rapid growth of the fetuses. Pregnant rats fed ad libitum also developed hypertriglyceridemia if the diet contained fat. This hyperlipemia, unlike that in the fasted rats, was not due to increased fat mobilization and was unaffected by insulin administration. It is concluded that the fractional clearance of blood triglycerides is greatly reduced during late pregnancy.