High-fat diet-induced hyperinsulinemia and tissue-specific insulin resistance in<i>Cry</i>-deficient mice

Barclay, Johanna L.; Shostak, Anton; Leliavski, Alexei; Tsang, Anthony H.; Jöhren, Olaf; Müller-Fielitz, Helge; Landgraf, Dominic; Naujokat, Nadine; Horst, Gijsbertus T. J. van der; Oster, H.

doi:10.1152/ajpendo.00512.2012

Cited by 137 publications

(107 citation statements)

References 58 publications

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“…CRY1, a key regulator of the inhibitory arm of circadian rhythmicity, has been implicated as a key modulator of the intrinsic liver clock: the Cry1 gene is rhythmically expressed, with higher protein levels seen during the transition from night to day, where CRY1 reduces hepatic gluconeogenesis [8]. Mice deficient in CRY1 that are kept on a high-fat diet gain less weight than their wild-type littermates despite comparable levels of energy intake, whereas mice deficient in both CRY1 and CRY2 are susceptible to obesity despite lower energy intake, and show enhanced insulin secretion [9,10]. When fed normal chow, mice deficient in CRY1 or CRY2 do not differ phenotypically from wild-type mice [10], whereas mice deficient in both CRY1 and CRY2 gain less fat mass and increase their basal metabolic rate.…”

Section: Discussionmentioning

confidence: 99%

“…In human islets, the expression of CRY2 mRNA has been shown to be negatively correlated with levels of glycated haemoglobin, and the expression of CRY2 mRNA was lower in participants with type 2 diabetes [7]. Several recently published studies have further indicated the importance of CRY2 and its circadian co-regulator CRY1 on glucose metabolism and energy homeostasis in mice [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Season-dependent associations of circadian rhythm-regulating loci (CRY1, CRY2 and MTNR1B) and glucose homeostasis: the GLACIER Study

et al. 2015

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Aims/hypothesis The association of single nucleotide polymorphisms (SNPs) proximal to CRY2 and MTNR1B with fasting glucose is well established. CRY1/2 and MTNR1B encode proteins that regulate circadian rhythmicity and influence energy metabolism. Here we tested whether season modified the relationship of these loci with blood glucose concentration. Methods SNPs rs8192440 (CRY1), rs11605924 (CRY2) and rs10830963 (MTNR1B) were genotyped in a prospective cohort study from northern Sweden (n=16,499). The number of hours of daylight exposure during the year ranged from 4.5 to 22 h daily. Owing to the non-linear distribution of daylight throughout the year, season was dichotomised based on the vernal and autumnal equinoxes. Effect modification was assessed using linear regression models fitted with a SNP × season interaction term, marginal effect terms and putative confounding variables, with fasting or 2 h glucose concentrations as outcomes. Results The rs8192440 (CRY1) variant was only associated with fasting glucose among participants (n=2,318) examined during the light season ( β=−0.04 mmol/l per A allele, 95% CI −0.08, −0.01, p=0.02, p interaction =0.01). In addition to the established association with fasting glucose, the rs11605924 (CRY2) and rs10830963 (MTNR1B) loci were associated with 2 h glucose concentrations ( β=0.07 mmol/l per A allele, 95% CI 0.03, 0.12, p=0.0008, n=9,605, and β=−0.11 mmol/l per G allele, 95% CI −0.15, −0.06, p<0.0001, n=9,517, respectively), but only in participants examined during the dark season ( p interaction =0.006 and 0.04, respectively). Repeated measures analyses including data collected 10 years after baseline (n=3,500) confirmed the results for the CRY1 locus ( p interaction =0.01). Conclusions/interpretation In summary, these observations suggest a biologically plausible season-dependent association between SNPs at CRY1, CRY2 and MTNR1B and glucose homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Season-dependent associations of circadian rhythm-regulating loci (CRY1, CRY2 and MTNR1B) and glucose homeostasis: the GLACIER Study

et al. 2015

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“…Insulin secretion from pancreatic beta cells is clock-gated, and disruption of the positive arm of the clock -CLOCK or BMAL1 -results in hypoinsulinemia (Marcheva et al 2010, Sadacca et al 2011, while disruption of the clock's negative regulators -PERs and CRYs -is associated with hyperinsulinemia (Zhao et al 2012, Barclay et al 2013. Insulin sensitivity is reduced in shift workers, and accompanied by increased beta cell activity, suggesting a pre-diabetic state (Esquirol et al 2012).…”

Section: Ghrelin and Insulinmentioning

confidence: 99%

Interactions between endocrine and circadian systems

Tsang¹,

Barclay

Oster

2013

Journal of Molecular Endocrinology

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100

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In most species, endogenous circadian clocks regulate 24-h rhythms of behavior and physiology. Clock disruption has been associated with decreased cognitive performance and increased propensity to develop obesity, diabetes, and cancer. Many hormonal factors show robust diurnal secretion rhythms, some of which are involved in mediating clock output from the brain to peripheral tissues. In this review, we describe the mechanisms of clock-hormone interaction in mammals, the contribution of different tissue oscillators to hormonal regulation, and how changes in circadian timing impinge on endocrine signalling and downstream processes. We further summarize recent findings suggesting that hormonal signals may feed back on circadian regulation and how this crosstalk interferes with physiological and metabolic homeostasis.

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“…While Cry double-mutant mice show dampened feeding rhythms on normal chow diet (NCD) and HFD, they are generally lighter and leaner than wild-type controls. 7,40,68 Under HFD, however, they rapidly gain weight despite a lower food intake compared to wild types. 40 This effect is explained by an enhanced potential of Cry-mutant adipocytes for lipid uptake and insulin-stimulated lipogenesis, making them highly susceptible to HFD-induced obesity.…”

Section: -60mentioning

confidence: 99%

“…36,[38][39][40] This example highlights the complex interaction of cellular adipose clocks with external signals (e.g., food composition and gender effects) in adipocyte differentiation.…”

mentioning

confidence: 99%

Circadian rhythms and clocks in adipose tissues: current insights

Kiehn¹,

Koch²,

Walter³

et al. 2017

CPT

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High-fat diet-induced hyperinsulinemia and tissue-specific insulin resistance inCry-deficient mice

Abstract: van der Horst GT, Oster H. High-fat diet-induced hyperinsulinemia and tissue-specific insulin resistance in Cry-deficient mice.

Cited by 137 publications

References 58 publications

Season-dependent associations of circadian rhythm-regulating loci (CRY1, CRY2 and MTNR1B) and glucose homeostasis: the GLACIER Study

Season-dependent associations of circadian rhythm-regulating loci (CRY1, CRY2 and MTNR1B) and glucose homeostasis: the GLACIER Study

Interactions between endocrine and circadian systems

Circadian rhythms and clocks in adipose tissues: current insights

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