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The close relationship between circadian rhythm disruption and poor metabolic status is becoming increasingly evident, but role of adipokines is poorly understood. Here we investigated adipocyte function and the metabolic status of mice with a global loss of the core clock gene  Bmal1  fed either a normal or a high fat diet (22% by weight).  Bmal1  null mice aged 2 months were killed across 24 hours and plasma adiponectin and leptin, and adipose tissue expression of  Adipoq ,  Lep ,  Retn  and  Nampt  mRNA measured. Glucose, insulin and pyruvate tolerance tests were conducted and the expression of liver glycolytic and gluconeogenic enzyme mRNA determined.  Bmal1  null mice displayed a pattern of increased plasma adiponectin and plasma leptin concentrations on both control and high fat diets.  Bmal1  null male and female mice displayed increased adiposity (1.8 fold and 2.3 fold respectively) on the normal diet, but the high fat diet did not exaggerate these differences. Despite normal glucose and insulin tolerance,  Bmal1  null mice had increased production of glucose from pyruvate, implying increased liver gluconeogenesis. The  Bmal1  null mice had arrhythmic clock gene expression in epigonadal fat and liver, and loss of rhythmic transcription of a range of metabolic genes. Furthermore, the expression of epigonadal fat  Adipoq ,  Retn ,  Nampt ,  AdipoR1  and  AdipoR2  and liver  Pfkfb3  mRNA were down-regulated. These results show for the first time that global loss of  Bmal1 , and the consequent arrhythmicity, results in compensatory changes in adipokines involved in the cellular control of glucose metabolism.

Global Loss of Bmal1 Expression Alters Adipose Tissue Hormones, Gene Expression and Glucose Metabolism