−/− Aims/hypothesis Cc2 mice lacking the gene encoding the malities at about 9 months of age. These include elevated carcinoembryonic-antigen-related cell adhesion molecule global fat mass, hyperinsulinaemia and insulin resistance (as 2(Cc2 [also known as Ceacam2]) exhibit hyperphagia that determined by glucose and insulin intolerance, fed leads to obesity and insulin resistance. This starts at hyperglycaemia and decreased insulin signalling pathways). 2 months of age in female mice. Male mutants maintain Pair-feeding experiments showed that insulin resistance re- normal body weight and insulin sensitivity until the last sulted from hyperphagia. Indirect calorimetry demonstrated age previously examined (7–8 months), owing to increased that older mutant male mice had compromised energy expen- sympathetic tone to white adipose tissue and energy expen- diture. Despite increased insulin secretion caused by Cc2 de- diture. The current study investigates whether insulin letion, chronic hyperinsulinaemia did not develop in mutant resistance develops in mutant male mice at a later age male mice until about 9 months of age, at which point insulin and whether this is accompanied by changes in insulin clearance began to decline substantially. This was probably homeostasis. mediated by a marked decrease in hepatic CEACAM1 Methods Insulin response was assessed by insulin and
Diabetologia – Springer Journals
Published: May 31, 2017
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