The researchers used a model for diet-induced obesity that has been used extensively alongside genetic models and has close parallels with obesity, increasingly found in humans who consume a high-fat, energy-rich diet. In this model, young (8-week old) male, age matched mice were age-divided into groups and housed individually in an air-conditioned room at 222XC with a 12 hour light: 12 hour dark cycle. Experimental animals had free access to drinking water and a high fat diet (45 percent fat, 20 percent protein and 35 percent carbohydrate; percent of total energy of 26.15kj/g). Age-matched control mice from the same colony had free access to a standard rodent maintenance diet (10 percent fat; 30 percent protein; 60 percent carbohydrate; percent of total energy of 12.99kj/g.). The two were used for comparison purposes.
Prior to the study, mice were maintained on a high fat diet for 160 days. In addition, a separate set of mice were maintained on a high fat diet for 112 days prior to measuring circulating GIP and GLP-1 levels. On both occasions, obesity and diabetes were clearly evident.
The mice which had previously been fed a high fat diet for 160 days received only daily injections of either saline or (Pro3)GIP over a 50-day period. Food intake and body weight were recorded daily while plasma glucose and insulin concentrations were monitored at 5-7 day intervals.
Blood was taken on day 50 to measure cholesterol, triglycerides, glucagon (the hormone involved in metabolizing carbohydrate), corticosterone (involved with carbohydrates in the liver) and circulating adipokines (which play a key role in obesity-related diseases). Glucose tolerance and insulin sensitivity tests were performed at the end of the study period. The metabolic response of both
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American Physiological Society