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Melanin-Concentrating Hormone Receptor 1 Deficiency Increases Insulin Sensitivity in Obese Leptin-Deficient Mice Without Affecting Body Weight

¹ Department of Physiology and Pharmacology, Gothenburg University, Gothenburg, Sweden
² AstraZeneca Transgenics & Comparative Genomics, AstraZeneca, Mölndal, Sweden
³ Department of Molecular Pharmacology, AstraZeneca, Mölndal, Sweden
⁴ Department of Integrative Pharmacology, AstraZeneca, Mölndal, Sweden
⁵ Department of Biostatistic, AstraZeneca, Mölndal, Sweden

Address correspondence and reprint requests to Mikael Bjursell, AstraZeneca, Mölndal S-43183 Mölndal, Sweden. E-mail: mikael.bjursell{at}astrazeneca.com

Abbreviations: BAT, brown adipose tissue; CRH, corticotrophin-releasing hormone; MCH, melanin-concentrating hormone; MCHr1, MCH receptor-1; MSH, melanocyte-stimulating hormone; RER, respiratory exchange ratio; SCD-1, stearoyl-CoA desaturase-1; UCP-1, uncoupling protein-1

The hypothalamic peptide melanin-concentrating hormone (MCH) plays important roles in energy homeostasis. Animals overexpressing MCH develop hyperphagia, obesity, and insulin resistance. In this study, mice lacking both the MCH receptor-1 (MCHr1 knockout) and leptin (ob/ob) double-null mice (MCHr1 knockout ob/ob) were generated to investigate whether the obesity and/or the insulin resistance linked to the obese phenotype of ob/ob mice was attenuated by ablation of the MCHr1 gene. In MCHr1 knockout ob/ob mice an oral glucose load resulted in a lower blood glucose response and markedly lower insulin levels compared with the ob/ob mice despite no differences in body weight, food intake, or energy expenditure. In addition, MCHr1 knockout ob/ob mice had higher locomotor activity and lean body mass, lower body fat mass, and altered body temperature regulation compared with ob/ob mice. In conclusion, MCHr1 is important for insulin sensitivity and/or secretion via a mechanism not dependent on decreased body weight.

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