Short-term feeding at the wrong time is sufficient to desynchronize peripheral clocks and induce obesity with hyperphagia, physical inactivity and metabolic disorders in mice

Yasumoto, Yuki; Hashimoto, Chiaki; Nakao, Reiko; Yamazaki, Haruka; Hiroyama, Hanako; Nemoto, Tadashi; Yamamoto, Saori; Sakurai, Mutsumi; Oike, Hideaki; Wada, Naoki; Yoshida-Noro, Chikako; Oishi, Katsutaka

doi:10.1016/j.metabol.2016.02.003

Cited by 139 publications

(114 citation statements)

References 40 publications

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“…Results of the present study are consistent with findings of daily rhythmic changes in the rates of absorption of saccharides in rat small intestine [33]. Feeding at an unusual time of day (inactive phase) desynchronizes peripheral clocks and causes obesity and metabolic disorders by inducing leptin resistance, hyperphagia, physical inactivity, hepatic fat accumulation and adiposity [34].…”

Section: Effects Of Growth Hormone On Dawn Phenomenon In Ratssupporting

confidence: 90%

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Shih¹,

Ho²

2016

J Diabetes Metab

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This review addresses the effects of growth hormone on diurnal insulin sensitivity in normal, patients with type 2 diabetes mellitus (T2DM) and animal models described in our previous studies. Results confirmed the presence of diurnal insulin sensitivity, or greater insulin sensitivity in the morning, in normal subjects. The exact cause of this circadian rhythm in plasma glucose levels in healthy subjects has not been established, and nocturnal surges in growth hormone secretion remain a possible explanation. Results showed that growth hormone is an important factor controlling the diurnal variation of glucose tolerance and insulin sensitivity in rats. Data from our previous study provided direct evidence that the role of growth hormone in regulating insulin sensitivity in healthy subjects may be related to changes in the metabolic clearance rate of insulin and the metabolism of non-esterified fatty acids. A different circadian rhythm for plasma glucose appears to be present in patients with T2DM with nadirs in the early evening and peaks in the early morning, indicating greater insulin sensitivity in the evening. As in normal subjects, the exact cause of these circadian rhythms in the plasma glucose levels of patients with T2DM provided direct evidence that the reduction in insulin sensitivity may be due to the nocturnal surge of growth hormone in the early morning hours.

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Section: Effects Of Growth Hormone On Dawn Phenomenon In Ratssupporting

confidence: 90%

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Shih¹,

Ho²

2016

J Diabetes Metab

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“…Furthermore, feeding mice at the wrong time (inactive or sleeping phase), desynchronizes peripheral clocks and causes obesity by inducing hyperphagia, physical inactivity, LEP resistance, hepatic lipid accumulation, and hyperadiposity. Liver and skeletal muscle metabolic rhythms become uncoupled as shown by temporal expression of desynchronized circadian clock genes in the skeletal muscle [81] .…”

Section: Circadian Clock Dysfunction and Obesitymentioning

confidence: 99%

White Adipose Tissue and Circadian Rhythm Dysfunctions in Obesity: Pathogenesis and Available Therapies

2016

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A combined neuroendocrine, metabolic, and chronobiological view can help to better understand the multiple and complex mechanisms involved in obesity development and maintenance, as well as to provide new effective approaches for its control and treatment. Indeed, we have currently updated data on the whole adipogenic process involved in white adipose tissue (WAT) mass expansion, namely due to a mechanism whereby WAT cells become hypertrophic, thus inducing a serious local (WAT) inflammatory condition that in turn, will impair not only the cross-talk between the hypothalamus and the WAT, but also favoring the development of deep and widespread neuroendocrine-metabolic dysfunction. Moreover, we also have revisited the circadian clock genes involved in dysfunctional WAT mass expansion and the mechanisms that may lead to obesity development, including early metabolic dysfunctions, enhanced oxidative stress and distorted energy homeostasis. The epigenetic changes of clock genes driving metabolic disease and obesity development have also been included in this review. Finally, we have also underlined the relevance of metabolic homeostasis regulation by central and peripheral organ clocks, sleep disturbances, nutrients, and feeding time, as key factors in obesity development as well as both, classical and chronotherapeutic approaches for its prevention and treatment.

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“…We found that the temporal expression of circadian clock genes in mice became synchronized in the liver, but not in skeletal muscle when feeding is restricted to 8 h/day during the light period. 35,36 We also found that RF inverts the circadian phase of plasma insulin, 35,36 suggesting that the circadian fluctuation of plasma insulin is not a dominant zeitgeber for the skeletal muscle clock. Nocturnal wheelrunning activity, body temperature, and corticosterone secretion were similar between mice fed only during the nighttime or the daytime under our experimental conditions.…”

Section: Function Of Feeding and Humoral Factors On Circadian Expressmentioning

confidence: 69%

“…Nocturnal wheelrunning activity, body temperature, and corticosterone secretion were similar between mice fed only during the nighttime or the daytime under our experimental conditions. 35 Neural signals from the central clock in the SCN, corticosterone, physical activity, and body temperature might be more potent zeitgebers for the skeletal muscle clock than feeding time and insulin, although intraperitoneally injected insulin induces Per1 and Per2 gene expression in mouse skeletal muscle. 36 Differences in tissue sensitivity to feeding time might cause desynchronization among molecular clocks in metabolic organs such as the liver and skeletal muscle, leading to disrupted metabolism.…”

Section: Function Of Feeding and Humoral Factors On Circadian Expressmentioning

confidence: 99%

The skeletal muscle circadian clock: current insights

Nakao¹,

Nikawa²,

Oishi³

2017

CPT

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Skeletal muscle functions in locomotion, postural support, and energy metabolism. The loss of skeletal muscle mass and function leads to diseases such as sarcopenia and metabolic disorders. Inactivity (lack of exercise) and an imbalanced diet (increased fat or decreased protein intake) are thought to be involved in the prevalence of such pathologies. On the other hand, recent epidemiological studies of humans have suggested that circadian disruption caused by shift work, jet lag, and sleep disorders is associated with obesity and metabolic syndrome. Experimental studies of mice deficient in clock genes have also identified skeletal muscle defects, suggesting a molecular link between circadian clock machinery and skeletal muscle physiology. Furthermore, accumulating evidence about chronotherapy, including chronopharmacology, chrononutrition, and chronoexercise, has indicated that timing is important to optimize medical intervention for various diseases. The present review addresses current understanding of the functional roles of the molecular clock with respect to skeletal muscle and the potential of chronotherapy for diseases associated with skeletal muscle.

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Short-term feeding at the wrong time is sufficient to desynchronize peripheral clocks and induce obesity with hyperphagia, physical inactivity and metabolic disorders in mice

Cited by 139 publications

References 40 publications

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models

White Adipose Tissue and Circadian Rhythm Dysfunctions in Obesity: Pathogenesis and Available Therapies

The skeletal muscle circadian clock: current insights

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