High-Fat Diet Delays and Fasting Advances the Circadian Expression of Adiponectin Signaling Components in Mouse Liver

Barnea, Maayan; Madar, Zecharia; Froy, Oren

doi:10.1210/en.2008-0944

Cited by 121 publications

(97 citation statements)

References 49 publications

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“…However, recent studies have shown that introduction of a high-fat diet to animals leads to rapid changes in both the period of locomotor activity in constant darkness and to increased food intake during the normal rest period under light-dark conditions [178]. These changes in behavioral rhythmicity correlated with disrupted clock gene expression within hypothalamus, liver, and adipose tissue, and as well as with altered cycling of hormones and nuclear hormone receptors involved in fuel utilization, such as leptin, thyroid stimulating hormone (TSH), and testosterone in mice, rats, and humans [178][179][180][181][182][183]. Furthermore, a high-fat diet modulates carbohydrate metabolism by amplifying circadian variation in glucose tolerance and insulin sensitivity [119].…”

Section: Effect Of High-fat Diet On Circadian Rhythmsmentioning

confidence: 99%

Circadian Signatures in Rat Liver: From Gene Expression to Pathways

Olds¹

2014

Sleep, Circadian Rhythms, and Metabolism

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Obesity has become a serious public health problem and a major risk factor for the development of illnesses, such as insulin resistance and hypertension. Attempts to understand the causes of obesity and develop new therapeutic strategies have mostly focused on caloric intake and energy expenditure. Recent studies have shown that the circadian clock controls energy homeostasis by regulating the circadian expression and/or activity of enzymes, hormones, and transport systems involved in metabolism. Moreover, disruption of circadian rhythms leads to obesity and metabolic disorders. Therefore, it is plausible that resetting of the circadian clock can be used as a new approach to attenuate obesity. Feeding regimens, such as restricted feeding (RF), calorie restriction (CR), and intermittent fasting (IF), provide a time cue and reset the circadian clock and lead to better health. In contrast, high-fat (HF) diet leads to disrupted circadian expression of metabolic factors and obesity. This paper focuses on circadian rhythms and their link to obesity.

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Section: Effect Of High-fat Diet On Circadian Rhythmsmentioning

confidence: 99%

Circadian Signatures in Rat Liver: From Gene Expression to Pathways

Olds¹

2014

Sleep, Circadian Rhythms, and Metabolism

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“…By contrast, only a few studies have investigated the relationship existing between different diets and circadian clock regulation in wild-type mice. The effect of administering high-fat diet on the expression of clock genes has so far been studied in different tissues (Kohsaka et al 2007;Barnea et al 2009;Hsieh et al 2010;Yanagihara et al 2006), but to date, alterations of clock gene expression in the gut following administration of high-fat diet in wild-type mice have never been reported.…”

Section: Gene Expressionmentioning

confidence: 99%

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

et al. 2013

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Mice fed long-term high-fat diets (HFD) are an established model for human metabolic disorders, such as obesity and diabetes. However, also the effects of shortterm HFD feeding should be investigated to understand which are the first events that trigger the onset of a predisease condition, the so-called metabolic syndrome, that increases the risk of developing clinical diseases. In this study, C57BL/6N mice were fed a control diet (CTR) or a HFD for 1 (T1) or 2 weeks (T2). Metabolic and histological effects were examined. Cecum transcriptomes of HFD and CTR mice were compared at T2 by microarray analysis. Differentially expressed genes were validated by real-time PCR in the cecum and in the liver. After 2 weeks of diet administration, HFD mice showed an altered expression pattern in only seven genes, four of which are involved in the circadian clock regulatory pathway. Real-time PCR confirmed microarray results of the cecum and revealed the same trend of clock gene expression changes in the liver. These findings suggest that clock genes may play an important role in early controlling gut output systems in response to HFD in mice and that their expression change may also represent an early signaling of the development of an intestinal pro-inflammatory status.

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“…35 Samples were run on an SDS-polyacrylamide gel (10% for AMPK and SIRT1, 7.5% for ACC) and subsequently proteins were transferred into a nitrocellulose membrane. Blots were incubated with mouse anti-AMPK/pAMPK/ACC/pACC (Cell Signaling Technology Inc., Danvers, MA, USA) or anti-SIRT1 (Millipore, Billerica, MA, USA) antibodies and after several washes with anti-rabbit IgG horseradish peroxidase-conjugated secondary antibody (Cell Signaling Technology Inc.).…”

Section: Western Blot Analysismentioning

confidence: 99%

Spontaneous caloric restriction associated with increased leptin levels in obesity-resistant αMUPA mice

et al. 2010

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Background: aMUPA mice carry as a transgene the cDNA encoding urokinase-type plasminogen activator, a member of the plasminogen/plasmin system that functions in fibrinolysis and extracellular proteolysis. These mice spontaneously consume less food when fed ad libitum and live longer compared with wild-type (WT) control mice. aMUPA mice are obesity resistant and they share many similarities with calorically restricted animals. However, extensive metabolic characterization of this unique transgenic model has never been performed. Method: Metabolism of aMUPA mice was analyzed by measuring hormone, lipid and glucose levels in the serum, as well as gene and protein expression levels in the liver, hypothalamus and brainstem. Results: aMUPA mice were found to be leaner than WT mice mainly because of reduced fat depots. Serum analyses showed that aMUPA mice have high levels of the anorexigenic hormones insulin and leptin, and low levels of the orexigenic hormone ghrelin. Analyses of brain neuropeptides showed that the transcript of the anorexigenic neuropeptide Pomc is highly expressed in the brainstem, whereas the expression of the orexigenic neuropeptides Npy, Orexin and Mch is blunted in the hypothalamus of aMUPA mice. In addition, adenosine monophosphate (AMP)-activated protein kinase (AMPK) levels were higher in the liver and lower in the hypothalamus, thus promoting simultaneously central reduction in appetite and peripheral loss of fat. The levels of SIRT1 were low in the liver, but high in the hypothalamus, a feature that aMUPA mice share with calorically restricted animals. Conclusion: Taken together, aMUPA mice exhibit a unique metabolic phenotype of low-calorie intake and high leptin levels, and could serve as a model for both spontaneous calorie restriction and resistance to obesity.

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High-Fat Diet Delays and Fasting Advances the Circadian Expression of Adiponectin Signaling Components in Mouse Liver

Cited by 121 publications

References 49 publications

Circadian Signatures in Rat Liver: From Gene Expression to Pathways

Circadian Signatures in Rat Liver: From Gene Expression to Pathways

The nutrigenomic investigation of C57BL/6N mice fed a short-term high-fat diet highlights early changes in clock genes expression

Spontaneous caloric restriction associated with increased leptin levels in obesity-resistant αMUPA mice

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