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Global loss of bmal1 expression alters adipose tissue hormones, gene expression and glucose metabolism.

Kennaway DJ, Varcoe TJ, Voultsios A, Boden MJ - PLoS ONE (2013)

Bottom Line: The close relationship between circadian rhythm disruption and poor metabolic status is becoming increasingly evident, but role of adipokines is poorly understood.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.

View Article: PubMed Central - PubMed

Affiliation: Robinson Institute, University of Adelaide, Adelaide, South Australia, Australia.

ABSTRACT
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 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 mice displayed a pattern of increased plasma adiponectin and plasma leptin concentrations on both control and high fat diets. Bmal1 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 mice had increased production of glucose from pyruvate, implying increased liver gluconeogenesis. The Bmal1 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.

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The blood glucose response to the intra peritoneal administration of pyruvate (2 mg/g) to male and female wild-type and Bmal1  mice fed a normal rodent diet.The mean ± s.e.m. plasma glucose levels are shown for male (a) and female (c) wild-type (open circles) and Bmal1  (closed circles) mice. The mean area under the curve (± SEM) of the plasma glucose profiles up to 120 min post injection (b, d).
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pone-0065255-g002: The blood glucose response to the intra peritoneal administration of pyruvate (2 mg/g) to male and female wild-type and Bmal1 mice fed a normal rodent diet.The mean ± s.e.m. plasma glucose levels are shown for male (a) and female (c) wild-type (open circles) and Bmal1 (closed circles) mice. The mean area under the curve (± SEM) of the plasma glucose profiles up to 120 min post injection (b, d).

Mentions: At 2 months of age, administration of pyruvate resulted in increased blood glucose levels in both male and female Bmal1 mice compared to wild type mice (Fig. 2). The blood glucose levels failed to return to the baseline within 120 minutes in either the wild-type or Bmal1 mice, but was significantly higher at 120 minutes post injection in Bmal1 mice compared to wild-type mice males (P<0.05), but not females.


Global loss of bmal1 expression alters adipose tissue hormones, gene expression and glucose metabolism.

Kennaway DJ, Varcoe TJ, Voultsios A, Boden MJ - PLoS ONE (2013)

The blood glucose response to the intra peritoneal administration of pyruvate (2 mg/g) to male and female wild-type and Bmal1  mice fed a normal rodent diet.The mean ± s.e.m. plasma glucose levels are shown for male (a) and female (c) wild-type (open circles) and Bmal1  (closed circles) mice. The mean area under the curve (± SEM) of the plasma glucose profiles up to 120 min post injection (b, d).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3672145&req=5

pone-0065255-g002: The blood glucose response to the intra peritoneal administration of pyruvate (2 mg/g) to male and female wild-type and Bmal1 mice fed a normal rodent diet.The mean ± s.e.m. plasma glucose levels are shown for male (a) and female (c) wild-type (open circles) and Bmal1 (closed circles) mice. The mean area under the curve (± SEM) of the plasma glucose profiles up to 120 min post injection (b, d).
Mentions: At 2 months of age, administration of pyruvate resulted in increased blood glucose levels in both male and female Bmal1 mice compared to wild type mice (Fig. 2). The blood glucose levels failed to return to the baseline within 120 minutes in either the wild-type or Bmal1 mice, but was significantly higher at 120 minutes post injection in Bmal1 mice compared to wild-type mice males (P<0.05), but not females.

Bottom Line: The close relationship between circadian rhythm disruption and poor metabolic status is becoming increasingly evident, but role of adipokines is poorly understood.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.

View Article: PubMed Central - PubMed

Affiliation: Robinson Institute, University of Adelaide, Adelaide, South Australia, Australia.

ABSTRACT
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 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 mice displayed a pattern of increased plasma adiponectin and plasma leptin concentrations on both control and high fat diets. Bmal1 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 mice had increased production of glucose from pyruvate, implying increased liver gluconeogenesis. The Bmal1 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.

Show MeSH
Related in: MedlinePlus