Objective: Measurement of energy intake in lean mice, diet-induced obesity mice, and ob/ob obese mice after GHS-R antagonist administration
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Background and aims: Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R), is an appetite stimulatory signal from the stomach with structural resemblance to motilin. We examined the effects of the gastric peptide ghrelin and GHS-R antagonists on energy balance and glycaemic control in mice. Materials and methods: Body weight, fat mass, glucose, insulin, and gene expression of leptin, adiponectin, and resistin in white adipose tissue (WAT) were measured after repeated administrations of ghrelin under a high fat diet. Gastric ghrelin gene expression was assessed by northern blot analysis. Energy intake and gastric emptying were measured after administration of GHS-R antagonists. Repeated administration of GHS-R antagonist was continued for six days in ob/ob obese mice. Results: Ghrelin induced remarkable adiposity and worsened glycaemic control under a high fat diet. Pair feeding inhibited this effect. Ghrelin elevated leptin mRNA expression and reduced resistin mRNA expression. Gastric ghrelin mRNA expression during fasting was increased by a high fat diet. GHS-R antagonists decreased energy intake in lean mice, in mice with diet induced obesity, and in ob/ob obese mice; it also reduced the rate of gastric emptying. Repeated administration of GHS-R antagonist decreased body weight gain and improved glycaemic control in ob/ob obese mice. Conclusions: Ghrelin appears to be closely related to excess weight gain, adiposity, and insulin resistance, particularly under a high fat diet and in the dynamic stage. Gastric peptide ghrelin and GHS-R may be promising therapeutic targets not only for anorexia-cachexia but also for obesity and type 2 diabetes, which are becoming increasingly prevalent worldwide.
Administer GHS-R antagonist to lean mice, diet-induced obesity mice, and ob/ob obese mice
Note: For repeated administration studies, continued for six days in ob/ob obese mice
“Energy intake and gastric emptying were measured after administration of GHS-R antagonists”
Measure food consumption and energy intake in all three mouse groups following GHS-R antagonist administration
Note: GHS-R antagonists decreased energy intake in lean mice, diet-induced obesity mice, and ob/ob obese mice
“GHS-R antagonists decreased energy intake in lean mice, in mice with diet induced obesity, and in ob/ob obese mice”
Assess the rate of gastric emptying following GHS-R antagonist administration
Note: GHS-R antagonists reduced the rate of gastric emptying
“it also reduced the rate of gastric emptying”
Continue GHS-R antagonist administration for six days in ob/ob obese mice
Note: Repeated administration decreased body weight gain and improved glycaemic control
“Repeated administration of GHS-R antagonist was continued for six days in ob/ob obese mice”
Monitor body weight changes in ob/ob obese mice following repeated GHS-R antagonist administration
Note: Repeated administration decreased body weight gain
“Repeated administration of GHS-R antagonist decreased body weight gain”
Measure glucose levels and glycaemic control in ob/ob obese mice after repeated GHS-R antagonist administration
Note: Repeated administration improved glycaemic control in ob/ob obese mice
“Repeated administration of GHS-R antagonist decreased body weight gain and improved glycaemic control in ob/ob obese mice”
Three groups tested: lean mice, diet-induced obesity mice, and ob/ob obese mice