Obesity alters the expression profile of clock genes in peripheral blood mononuclear cells. Preliminary results

Tahira, Kazunobu; Ueno, Takayoshi; Fukuda, Noboru; Aoyama, T.; Tsunemi, Akiko; Matsumoto, Siroh; Nagura, Chinami; Matsumoto, Tarô; Soma, Masayoshi; Shimba, Shigeki; Matsumoto, Yoshiaki

doi:10.5114/aoms.2011.26603

Cited by 30 publications

(23 citation statements)

References 34 publications

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“…Mice lacking a functional leptin gene (ob/ob mice) have disrupted clock gene expression in both adipose tissue and liver , and rats with disrupted leptin signalling show tissue-specific alterations of clock gene expression . Even humans fed a high-fat diet have suppressed clock gene rhythms in adipose tissue, which parallels the disrupted leptin rhythms (Tahira et al 2011). Similarly, in mice, a high-fat diet dampens the rhythmicity of clock gene expression in the adipose tissue, liver, and brainstem (Kaneko et al 2009;Kohsaka et al 2007).…”

Section: Leptinmentioning

confidence: 97%

Circadian Clocks and Inflammation: Reciprocal Regulation and Shared Mediators

Cermakian

Westfall

Kiessling

2014

Arch. Immunol. Ther. Exp.

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The immune system is deeply interconnected with the endogenous 24-h oscillators of the circadian system. Indeed, the connection between these two physiological systems occurs at multiple levels and in both directions. On one hand, various aspects of the immune system show daily rhythms, which appear to be essential for healthy immune maintenance and proper immune response. On the other hand, immune responses cause changes in circadian rhythms, disrupting their delicate balance and manifesting in disease. Indeed, immune challenges cause various time-, gene-, and tissue-specific effects on circadian-regulated factors. This article reviews the possible mediators of the cross talk between the circadian clock and the immune system, in particular the inflammatory pathways. The rhythmic expression of cytokines and their receptors, as well as other rhythmically regulated humoral factors such as glucocorticoids, melatonin, leptin, or prostaglandins, could gate the effects of the immune response on the circadian system. In addition, systemic cues such as body temperature and neuronal connections between the brain and peripheral tissues may underlie the immune-circadian communication.

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Section: Leptinmentioning

confidence: 97%

Circadian Clocks and Inflammation: Reciprocal Regulation and Shared Mediators

Cermakian

Westfall

Kiessling

2014

Arch. Immunol. Ther. Exp.

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“…The patient groups were small and therefore some results could not reach or were bordering on statistical significance. Also we could not evaluate sex-dependent differences in both groups because of too few patients, especially in group C. Therefore further detailed studies based on a larger population are needed for a more comprehensive evaluation [28][29][30][31][32][33][34][35][36].…”

Section: Discussionmentioning

confidence: 99%

Serum concentrations of adiponectin, leptin, resistin, ghrelin and insulin and their association with obesity indices in obese normo- and hypertensive patients – pilot study

Stępień¹,

Wlazeł²,

Paradowski³

et al. 2012

aoms

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A b s t r a c tIntroduction: Hypertension often coexists with obesity. Adipokines, ghrelin and insulin play important roles in the pathogenesis of both diseases. The aim of this study was to compare adiponectin, leptin, resistin, insulin and ghrelin mean serum concentrations and insulin resistance (HOMA-IR) in normo-and hypertensive patients with obesity. Material and methods: All included patients were divided on the following groups: non-diabetic hypertensive patients with class I obesity (group A, n = 21) and class II/III obesity (group B, n = 10), and normotensive obese (class I)patients (group C, n = 7). Correlations between obesity indices (body mass index [BMI], waist-tohip ratio [WHR], waist circumference [WC]), HOMA-IR, and hormone and adipokine serum levels were also analyzed. Results: Leptin level and HOMA-IR were significantly higher in group B compared to group C (9.74 ±3.88 ng/ml vs. 4.53 ±3.00 ng/ml; p < 0.02 and 3.30 ±1.59 vs. 1.65 ±0.41; p < 0.02, respectively). A negative correlation between WC and adiponectin level (R = -0.6275; p < 0.01) and a positive correlation between WC and insulin concentration (R = 0.5122; p < 0.05) as well as with HOMA-IR (R = 0.5228; p < 0.02) were found in group A. Negative correlations between BMI and ghrelin level (R = -0.7052; p < 0.05), WHR and adiponectin level (R = -0.6912; p < 0.05) and WHR and leptin level (R = -0.6728; p < 0.05) were observed in group B. Conclusions: Insulin resistance and leptin may be important pathogenic factors in hypertensive patients with severe obesity. Indices of abdominal obesity (WC, WHR) correlate better than BMI with HOMA-IR, insulin, adiponectin and leptin serum levels in hypertensive obese patients.

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“…The SNPs and deregulation of human Per genes are also linked to obesity, metabolic syndromes, type 2 diabetes, eating, mood and sleep disorders, cardiovascular diseases, aging, depression, chronic inflammation, and neurodegeneration (98, 99, 134, 164, 169, 170, 197, 229–240). …”

Section: The Circadian Genes In Cancermentioning

confidence: 99%

Circadian gene variants in cancer

2014

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Humans as diurnal beings are active during the day and rest at night. This daily oscillation of behavior and physiology is driven by an endogenous circadian clock not environmental cues. In modern societies, changes in lifestyle have led to a frequent disruption of the endogenous circadian homeostasis leading to increased risk of various diseases including cancer. The clock is operated by the feedback loops of circadian genes and controls daily physiology by coupling cell proliferation and metabolism, DNA damage repair, and apoptosis in peripheral tissues with physical activity, energy homeostasis, immune and neuroendocrine functions at the organismal level. Recent studies have revealed that defects in circadian genes due to targeted gene ablation in animal models or single nucleotide polymorphism, deletion, deregulation and/or epigenetic silencing in humans are closely associated with increased risk of cancer. In addition, disruption of circadian rhythm can disrupt the molecular clock in peripheral tissues in the absence of circadian gene mutations. Circadian disruption has recently been recognized as an independent cancer risk factor. Further study of the mechanism of clock-controlled tumor suppression will have a significant impact on human health by improving the efficiencies of cancer prevention and treatment.

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Obesity alters the expression profile of clock genes in peripheral blood mononuclear cells. Preliminary results

Cited by 30 publications

References 34 publications

Circadian Clocks and Inflammation: Reciprocal Regulation and Shared Mediators

Circadian Clocks and Inflammation: Reciprocal Regulation and Shared Mediators

Serum concentrations of adiponectin, leptin, resistin, ghrelin and insulin and their association with obesity indices in obese normo- and hypertensive patients – pilot study

Circadian gene variants in cancer

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