Stomach secretes estrogen in response to the blood triglyceride levels

Mammals receive body energy information to maintain energy homeostasis. Ghrelin, insulin, leptin and vagal afferents transmit the status of fasting, blood glucose, body fat, and food intake, respectively. Estrogen also inhibits feeding behavior and lipogenesis, but increases body fat mass. However, how blood triglyceride levels are monitored and the physiological roles of estrogen from the perspective of lipid homeostasis remain unsettled. Here, we show that stomach secretes estrogen in response to the blood triglyceride levels. Estrogen-secreting gastric parietal cells predominantly use fatty acids as an energy source. Blood estrogen levels increase as blood triglyceride levels rise in a stomach-dependent manner. Estrogen levels in stomach tissues increase as blood triglyceride levels rise, and isolated gastric gland epithelium produces estrogen in a fatty acid-dependent manner. We therefore propose that stomach monitors and controls blood triglyceride levels using estrogen, which inhibits feeding behavior and lipogenesis, and promotes triglyceride uptake by adipocytes.

Protective Effect of Prunus Dulcis Against Acetylsalicylic Acid Injury on Gastric Parietal Cells

Background: Acetylsalicylic acid is in common clinical use but has the side effect of causing gastric mucosal erosions and selective injury to parietal cells. Aim: To explore if prior treatment with Prunus dulcis (almond) had a protective effect against acetylsalicylic acid induced injury. Study design: Experimental study. Methodology: Albino mice weighing 30 to 40 grams were given two drops of almond oil without peel and 300 mg of finely ground whole almond kernel by oral gavage for sixty days followed by 400 mg/kg body weight of acetylsalicylic acid orally. Gastric mucosal damage was observed and recorded as ulcer index. The number of parietal cells/ sq. micrometer and area of parietal cells were observed and recorded under microscope in formalin fixed H and E stained sections. Data analyzed by SPSS 22.0v. Results: Mucosal damage, distortion of gastric glands and damage to parietal cells was pronounced in the positive control animals. The number of surviving parietal cells after acetylsalicylic acid insult in animals given almond oil was significantly higher when compared with positive control animals (p<0.001) and even better in animals receiving whole ground almond kernel. The area of parietal cells was also similarly larger in the treated animals. Conclusion: This study concluded Prunus dulcis offers protection against acute gastric mucosal injury and damage to the gastric parietal cells caused by acetylsalicylic acid in mice. Keywords: Prunus Dulcis, Parietal Cells, Gastric Erosions and Acetylsalicylic Acid.

Stomach secretes estrogen in response to blood triglyceride levels in males

The central nervous system receives body energy information and controls feeding behavior and lipogenesis1. Ghrelin, insulin, leptin and vagal afferents transmit the status of fasting, blood glucose, body fat, and food intake, respectively2-5. Estrogen, which is secreted from adipocytes and gastric parietal cells and from the ovaries in females, also acts upon the central nervous system and liver to inhibit feeding behavior and lipogenesis6-9. How blood triglyceride levels are monitored and how estrogen levels are regulated from the perspective of the lipid homeostasis is not well understood. Using male rats, we show that gastric parietal cells secrete estrogen in response to blood triglyceride levels. Parietal cells predominantly use fatty acid as an energy source. When male rats are administered olive oil or glucose, blood estrogen levels increase as the blood triglyceride, but not glucose, levels rise. Estrogen levels in stomach tissues increase as the blood triglyceride levels rise, and blood triglyceride level-dependent increases of blood estrogen levels are cancelled in gastrectomized rats. We therefore propose that in males, parietal cells in the stomach act as a sensor for the blood triglyceride levels and can secrete estrogen to inhibit the hepatic lipogenesis and feeding behavior when blood triglyceride levels are high.

Modeling acute ethanol-induced impairment with gastric organoids

Background: Ethanol has been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeleton interactions in gastric parietal cells and thereby caused hypochlorhydria.

Stomach-specific c-Myc overexpression drives gastric adenoma in mice via AKT/mTOR signaling

Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc transgenic mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce gastric adenoma in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric tumorigenesis can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.

Modeling Acute Ethanol-Induced Impairment with Gastric Organoids

Background: Ethanol have been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeletal interactions in gastric parietal cells and thereby caused hypochlorhydria.

Induction of Erythrocyte Shrinkage by Omeprazole

Omeprazole, a proton pump inhibitor blocks the H+/K+-ATPase channels of gastric parietal cells. It is used for the treatment of peptic ulcer. Prolonged use of omeprazole may involve in inducing anemia. The key marker of eryptosis includes membrane blebbing, cell shrinkage and phosphatidylserine (PS) exposure at the cell surface. In current study, the eryptotic, oxidative as well as hemolytic effects of therapeutical doses (0.5, 1 and 1.5 µM) of omeprazole were investigated after exposing erythrocytes for 48 hours. Investigation of eryptosis was done by cell size measurement, PS exposure determination and calcium channel inhibition. As a possible mechanism of omeprazole induced eryptosis, oxidative stress was investigated by determining the catalase, glutathione peroxidase and superoxide dismutase activities. Similarly, necrotic effect of omeprazole on erythrocytes was also evaluated through hemolysis measurement. Results of our study illustrated that 1.5 µM of omeprazole may induce significant decrease in superoxide dismutase, glutathione peroxidase and catalase activities as well as triggered the erythrocytes shrinkage, PS exposure and hemolysis. Role of calcium was also confirmed in inducing erythrocyte shrinkage. It is concluded that the exposure of erythrocytes with 1.5 µM omeprazole may enhance the rate of eryptosis and hemolysis by inducing oxidative stress.

Stomach

The stomach develops during the fifth week of gestation from the dilated caudal portion of the foregut. The gastric cardia is just distal to the gastroesophageal junction, the fundus is the upper curvature to the left of the cardia, the body is the central region between the fundus and antrum, and the antrum tapers into the pylorus. Gastric parietal cells secrete hydrochloric acid and intrinsic factor, chief cells secrete pepsinogen, and G cells secrete gastrin. PUD is the most common cause of massive UGI bleeding. Although a UGI series can be used for diagnosis of gastric lesions, some are indistinguishable from benign peptic ulcers. Possible complications of gastric surgery include bleeding, anastomotic leak or stricture, or reflux esophagitis.