Abstract
Gastric parietal cells (gastric acid secreting cells) secrete estrogen in response to blood lipid (triglycerides and fatty acids) levels.1 Estrogen decreases blood lipids by suppressing appetite, lipogenesis and lipolysis and by increasing lipid storage and consumption,2–5 so gastric estrogen plays an important role in maintaining blood lipids levels.1 However, parietal cells use fatty acids to generate energy for estrogen production and acid secretion, so postprandial changes in blood lipid levels and acid secretion activities could affect production of gastric estrogen. Here we show that blood estrogen decreases after meals, especially after carbohydrate intake. Blood fatty acids also decrease, and intravenous injection of lipids partially restores blood estrogen levels. Gastric acid-secreting hormones decrease production of gastric estrogen, while antacid and gastric acid-suppressing hormones, including those secreted after lipid ingestion like glucagon-like peptide-1 (GLP-1),6 increase gastric estrogen production and postprandially decreased blood estrogen levels. Secreted insulin and gastric estrogen directly enter the liver to enhance and suppress lipogenesis respectively,7 before diluted in the systemic blood. We therefore conclude that diet and the subsequently secreted hormones regulate gastric estrogen production, as well as insulin secretion, for proper hepatic lipogenesis, taking into account ingested carbohydrate and lipid levels.