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  • SAGE Publications  (6)
  • Biodiversity Research  (6)
  • 1
    Online Resource
    Online Resource
    SAGE Publications ; 2011
    In:  Journal of Biological Rhythms Vol. 26, No. 2 ( 2011-04), p. 99-106
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 26, No. 2 ( 2011-04), p. 99-106
    Abstract: The mammalian circadian clock in the suprachiasmatic nucleus (SCN) drives and maintains 24-h physiological rhythms, the phases of which are set by the local environmental light-dark cycle. Gastrin-releasing peptide (GRP) communicates photic phase setting signals in the SCN by increasing neurophysiological activity of SCN neurons. Here, the ionic basis for persistent GRP-induced changes in neuronal activity was investigated in SCN slice cultures from Per1::GFP reporter mice during the early night. Recordings from Per1 -fluorescent neurons in SCN slices several hours after GRP treatment revealed a significantly greater action potential frequency, a significant increase in voltage-activated outward current at depolarized potentials, and a significant increase in 4-aminopyridine—sensitive fast delayed rectifier (fDR) potassium currents when compared to vehicle-treated slices. In addition, the persistent increase in spike rate following early-night GRP application was blocked in SCN neurons from mice deficient in Kv3 channel proteins. Because fDR currents are regulated by the clock and are elevated in amplitude during the day, the present results support the model that GRP delays the phase of the clock during the early night by prolonging day-like membrane properties of SCN cells. Furthermore, these findings implicate fDR currents in the ionic basis for GRP-mediated entrainment of the primary mammalian circadian pacemaker.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 2018064-0
    SSG: 12
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  • 2
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 22, No. 4 ( 2007-08), p. 324-334
    Abstract: Spot14 is a putative transcriptional regulator for genes involved in fatty acid synthesis. The Spot14 gene is activated in response to lipogenic stimuli such as dietary carbohydrate and is also under circadian regulation. The authors investigated factors responsible for daily oscillation of Spot14 expression. If mice were kept under a 12-h light/12-h dark cycle with ad libitum feeding, Spot14 mRNA levels in the liver reached a peak at an early dark period when mice, as nocturnal animals, start feeding. Under fasting, while Spot14 mRNA levels were generally decreased, the rhythmicity was still maintained, suggesting contribution of both nutritional elements and circadian clock factors on robust rhythmicity of Spot14 expression. Effects of circadian clock factors were confirmed by the observations that the circadian rhythm of Spot14 expression was seen also under the constant darkness and that the rhythmicity was lost in Clock mutant mice. When mice were housed in short-photoperiod (6-h light/18-h dark) and long-photoperiod (18-h light/6-h dark) cycles, rhythms of Spot14 mRNA levels were phase advanced and phase delayed, respectively, being concordant with the notion that Spot14 expression is under the control of the light-entrainable oscillator. As for nutritional mediators, in the liver of db/ db mice exhibiting hyperinsulinemia-accompanied hyperglycemia, Spot14 mRNA levels were constantly high without apparent rhythmicity, consistent with previous observations for strong activation of the Spot14 gene by glucose and insulin. Restricted feeding during the 4-h mid-light period caused a phase advance of the Spot14 expression rhythm. On the other hand, restricted feeding during the 4-h mid-dark period led to damping of the rhythmicity, apparently resulting from the separation of phases between effects of the light/dark cycle and feeding on Spot14 expression. Thus, the daily rhythm of Spot14 expression in the liver is under the control of the light-entrainable oscillator, food-entrainable oscillator, and food-derived nutrients, in a separate or cooperative manner.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2007
    detail.hit.zdb_id: 2018064-0
    SSG: 12
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  • 3
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 25, No. 1 ( 2010-02), p. 9-18
    Abstract: Restricted feeding induces anticipatory activity rhythm and also entrains the peripheral circadian clocks, although the underlying brain mechanisms have not been fully elucidated. The dorsomedial hypothalamus (DMH) has been implicated in the regulation of restricted feeding—induced anticipatory activity rhythms (FAA), but the role of the DMH in restricted feeding— induced entrainment of peripheral circadian clocks is still unknown. In the present study, the role of the DMH in entrainment of the peripheral circadian clock was examined using Per2::luciferase knock-in mice. The results indicate that lesions that destroy the large mediobasal hypothalamic (MBH) lesions destroying the DMH, ventrolateral hypothalamus (VMH), and arcuate nucleus (ARC) significantly reduce daily locomotor activity rhythms and FAA formation. In addition, these lesions phase advanced the peak of liver Per2 expression by 2 h when compared to sham-operated mice. Following the administration of MBH lesions, the animals run less and start later in the restricted feeding— induced FAA rhythm but do not have any alterations in the restricted feeding— induced phase shift of the liver Per2 rhythm. These results demonstrate that the hypothalamus, including the MBH, is an important brain area for maintaining the locomotor rhythm and FAA formation. However, it is not necessary for restricted feeding—induced entrainment of the liver clock.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
    detail.hit.zdb_id: 2018064-0
    SSG: 12
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  • 4
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 26, No. 3 ( 2011-06), p. 200-209
    Abstract: The neuropeptide vasoactive intestinal polypeptide (VIP) has emerged as a key candidate molecule mediating the synchronization of rhythms in clock gene expression within the suprachiasmatic nucleus (SCN). In addition, neurons expressing VIP are anatomically well positioned to mediate communication between the SCN and peripheral oscillators. In this study, we examined the temporal expression profile of 3 key circadian genes: Per1, Per2 , and Bmal1 in the SCN, the adrenal glands and the liver of mice deficient for the Vip gene (VIP KO), and their wild-type counterparts. We performed these measurements in mice held in a light/dark cycle as well as in constant darkness and found that rhythms in gene expression were greatly attenuated in the VIP-deficient SCN. In the periphery, the impact of the loss of VIP varied with the tissue and gene measured. In the adrenals, rhythms in Per1 were lost in VIP-deficient mice, while in the liver, the most dramatic impact was on the phase of the diurnal expression rhythms. Finally, we examined the effects of the loss of VIP on ex vivo explants of the same central and peripheral oscillators using the PER2::LUC reporter system. The VIP-deficient mice exhibited low amplitude rhythms in the SCN as well as altered phase relationships between the SCN and the peripheral oscillators. Together, these data suggest that VIP is critical for robust rhythms in clock gene expression in the SCN and some peripheral organs and that the absence of this peptide alters both the amplitude of circadian rhythms as well as the phase relationships between the rhythms in the SCN and periphery.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 2018064-0
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    SAGE Publications ; 2007
    In:  Journal of Biological Rhythms Vol. 22, No. 4 ( 2007-08), p. 312-323
    In: Journal of Biological Rhythms, SAGE Publications, Vol. 22, No. 4 ( 2007-08), p. 312-323
    Abstract: Energy homeostasis is subjected to a circadian control that synchronizes energy intake and expenditure. The transcription factor CLOCK, a key component of the molecular circadian clock, controls many kinds of rhythms, such as those for locomotor activity, body temperature, and metabolic functions. The purpose of the present study is to understand the function of the Clock gene during lipid metabolism in the liver using Clock-mutant mice. Clock-mutant mice with an ICR background were fed a high-fat diet for 13 weeks, and liver triglyceride, serum triglyceride, and serum free fatty acid levels were examined. Triglyceride content in the liver was significantly less increased in Clock-mutant mice on a high-fat diet compared to wild-type mice on a high-fat diet. Acsl4 and Fabp1 mRNA levels in the liver showed daily rhythms in wild-type mice. In contrast, Clock -mutant mice had attenuated daily rhythms of Acsl4 and Fabp1 gene expression in the liver under both normal and high-fat diet conditions compared to wild-type mice. In Clock-mutant mice, suppression of Acsl4 and Fabp1 mRNA in the liver under high-fat diet conditions may have attenuated the accumulation of triglycerides in the liver compared to wild-type mice under the same conditions. In conclusion, the authors demonstrate that mice with a Clock mutation showed less triglyceride accumulation in the liver through the suppression of Acsl4 and Fabp1 gene expression when fed a high-fat diet compared to wild-type mice fed the same diet.
    Type of Medium: Online Resource
    ISSN: 0748-7304 , 1552-4531
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2007
    detail.hit.zdb_id: 2018064-0
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    SAGE Publications ; 2007
    In:  Evolutionary Bioinformatics Vol. 3 ( 2007-01), p. 117693430700300-
    In: Evolutionary Bioinformatics, SAGE Publications, Vol. 3 ( 2007-01), p. 117693430700300-
    Abstract: This study was undertaken to clarify the molecular basis for human skin color variation and the environmental adaptability to ultraviolet irradiation, with the ultimate goal of predicting the impact of changes in future environments on human health risk. One hundred twenty-two Caucasians living in Toledo, Ohio participated. Back and cheek skin were assayed for melanin as a quantitative trait marker. Buccal cell samples were collected and used for DNA extraction. DNA was used for SNP genotyping using the Masscode™ system, which entails two-step PCR amplification and a platform chemistry which allows cleavable mass spectrometry tags. The results show gene-gene interaction between SNP alleles at multiple loci (not necessarily on the same chromosome) contributes to inter-individual skin color variation while suggesting a high probability of linkage disequilibrium. Confirmation of these findings requires further study with other ethic groups to analyze the associations between SNP alleles at multiple loci and human skin color variation. Our overarching goal is to use remote sensing data to clarify the interaction between atmospheric environments and SNP allelic frequency and investigate human adaptability to ultraviolet irradiation. Such information should greatly assist in the prediction of the health effects of future environmental changes such as ozone depletion and increased ultraviolet exposure. If such health effects are to some extent predictable, it might be possible to prepare for such changes in advance and thus reduce the extent of their impact.
    Type of Medium: Online Resource
    ISSN: 1176-9343 , 1176-9343
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2007
    detail.hit.zdb_id: 2227610-5
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