Central administration of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide differentially regulates energy metabolism in chicks

Tachibana, Tetsuya; Oikawa, Daichi; Adachi, Nami; Boswell, Tim; Furuse, Mitsuhiro

doi:10.1016/j.cbpa.2006.12.043

Cited by 19 publications

(10 citation statements)

References 21 publications

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“…These results first demonstrated that deletion of Pacap had no significant effect on RMR of conscious, unstrained Pacap K/K mice housed at either 24 or 4 8C when compared with Pacap C/C mice as evidenced by similar O 2 consumption. This finding is at odds with previous reports demonstrating that administration of pharmacological PACAP (6-38), a PAC1 receptor antagonist, reduced energy expenditure (Tachibana et al 2007, Inglott et al 2011. Failure to detect a RMR difference between Pacap K/K and Pacap C/C mice may relate to our experimental approach, which measured oxygen consumption in conscious, unrestrained mice that were housed below thermoneutrality (28-30 8C).…”

Section: Discussioncontrasting

confidence: 54%

PACAP is essential for the adaptive thermogenic response of brown adipose tissue to cold exposure

Diané¹,

Nikolic²,

Rudecki³

et al. 2014

Journal of Endocrinology

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Pituitary adenylate cyclase-activating polypeptide (PACAP) is a widely distributed neuropeptide that acts as a neurotransmitter, neuromodulator, neurotropic factor, neuroprotectant, secretagogue, and neurohormone. Owing to its pleiotropic biological actions, knockout of Pacap (Adcyap1) has been shown to induce several abnormalities in mice such as impaired thermoregulation. However, the underlying physiological and molecular mechanisms remain unclear. A previous report has shown that cold-exposed Pacap null mice cannot supply appropriate levels of norepinephrine (NE) to brown adipocytes. Therefore, we hypothesized that exogenous NE would rescue the impaired thermogenic response of Pacap null mice during cold exposure. We compared the adaptive thermogenic capacity of Pacap K/K to Pacap C/C mice in response to NE when housed at room temperature (24 8C) and after a 3.5-week cold exposure (4 8C). Biochemical parameters, expression of thermogenic genes, and morphological properties of brown adipose tissue (BAT) and white adipose tissue (WAT) were also characterized. Results showed that there was a significant effect of temperature, but no effect of genotype, on the resting metabolic rate in conscious, unrestrained mice. However, the normal cold-induced increase in the basal metabolic rate and NE-induced increase in thermogenesis were severely blunted in cold-exposed Pacap K/K mice. These changes were associated with altered substrate utilization, reduced b 3 -adrenergic receptor (b 3 -Ar (Adrb3)) and hormone-sensitive lipase (Hsl (Lipe)) gene expression, and increased fibroblast growth factor 2 (Fgf2) gene expression in BAT. Interestingly, Pacap K/K mice had depleted WAT depots, associated with upregulated uncoupling protein 1 expression in inguinal WATs. These results suggest that the impairment of adaptive thermogenesis in Pacap null mice cannot be rescued by exogenous NE perhaps in part due to decreased b 3 -Ar-mediated BAT activation.

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Section: Discussioncontrasting

confidence: 54%

PACAP is essential for the adaptive thermogenic response of brown adipose tissue to cold exposure

Diané¹,

Nikolic²,

Rudecki³

et al. 2014

Journal of Endocrinology

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“…) and lipid utilization, while inhibiting feeding behavior (Tachibana et al. , ). PACAP could cause a phase shift of the endogenous oscillators from day‐to‐night activity through melatonin modulation, a major determinant of migration onset in passerines (Fusani and Gwinner ; Mueller et al.…”

Section: Discussionmentioning

confidence: 99%

“…Second, PACAP may affect migratory restlessness, and hence, the distance to be migrated from different breeding latitudes in autumn, by modulating melatonin secretion (Simonneaux et al 1993) and lipid utilization, while inhibiting feeding behavior (Tachibana et al 2003(Tachibana et al , 2007. PACAP could cause a phase shift of the endogenous oscillators from day-to-night activity through melatonin modulation, a major determinant of migration onset in passerines (Fusani and Gwinner 2005;Mueller et al 2011), and a fuel shift to lipid metabolism, which may influence nutritional state and night migratory activity (Coppack and Bairlein 2011;Schwartz and Andrews 2013).…”

Section: Potential Mechanisms Driving the Association Between Adcyap1mentioning

confidence: 99%

Adcyap1 polymorphism covaries with breeding latitude in a Nearctic migratory songbird, the Wilson's warbler (Cardellina pusilla)

Bazzi

Galimberti

Hays

et al. 2016

Ecology and Evolution

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Understanding the genetic background of complex behavioral traits, showing multigenic control and extensive environmental effects, is a challenging task. Among such traits, migration is known to show a large additive genetic component. Yet, the identification of specific genes or gene regions explaining phenotypic variance in migratory behavior has received less attention. Migration ultimately depends on seasonal cycles, and polymorphism at phenological candidate genes may underlie variation in timing of migration or other aspects of migratory behavior. In this study of a Nearctic-Neotropical migratory songbird, the Wilson's warbler (Cardellina pusilla), we investigated the association between polymorphism at two phenological candidate genes, Clock and Adcyap1, and two aspects of the migratory phenotype, timing of spring migration through a stopover site and inferred latitude of the breeding destination. The breeding destination of migrating individuals was identified using feather deuterium ratio (d 2 H), which reliably reflects breeding latitude throughout the species' western breeding range. Ninety-eight percent of the individuals were homozygous at Clock, and the rare heterozygotes did not deviate from homozygous migration phenology. Adcyap1 was highly polymorphic, and allele size was not significantly associated with migration date. However, Adcyap1 allele size significantly positively predicted the inferred breeding latitude of males but not of females. Moreover, we found a strong positive association between inferred breeding latitude and Adcyap1 allele size in long-distance migrating birds from the northern sector of the breeding range (western Canada), while this was not the case in short-distance migrating birds from the southern sector of the breeding range (coastal California). Our findings support previous evidence for a role of Adcyap1 in shaping the avian migratory phenotype, while highlighting that patterns of phenological candidate gene-phenotype associations may be complex, significantly varying between geographically distinct populations and even between the sexes.

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“…In the periphery, VIP may affect glucose metabolism at the level of the pancreas , the gastrointestinal tract and the liver . After central administration, VIP has been shown to decrease plasma glucose levels in 6‐day‐old chickens but to increase it in adult male Wistar rats . Moreover, Shimizu et al .…”

Section: Discussionmentioning

confidence: 99%

Suprachiasmatic Nucleus Neuropeptides and Their Control of Endogenous Glucose Production

Foppen

Tan

Ackermans

et al. 2016

J Neuroendocrinology

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Defective control of endogenous glucose production is an important factor responsible for hyperglycaemia in the diabetic individual. During the past decade, progressively more evidence has appeared indicating a strong and potentially causal relationship between disturbances of the circadian system and defects of metabolic regulation, including glucose metabolism. The detrimental effects of disturbed circadian rhythms may have their origin in disturbances of the molecular clock mechanisms in peripheral organs, such as the pancreas and liver, or in the central brain clock in the hypothalamic suprachiasmatic nuclei (SCN). To assess the role of SCN output per se on glucose metabolism, we investigated (i) the effect of several SCN neurotransmitters on endogenous glucose production and (ii) the effect of SCN neuronal activity on hepatic and systemic insulin sensitivity. We show that silencing of SCN neuronal activity results in decreased hepatic insulin sensitivity and increased peripheral insulin sensitivity. Furthermore, both oxytocin neurones in the paraventricular nucleus of the hypothalamus (PVN) and orexin neurones in the lateral hypothalamus may be important targets for the SCN control of glucose metabolism. These data further highlight the role of the central clock in the pathophysiology of insulin resistance.

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Central administration of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide differentially regulates energy metabolism in chicks

Cited by 19 publications

References 21 publications

PACAP is essential for the adaptive thermogenic response of brown adipose tissue to cold exposure

PACAP is essential for the adaptive thermogenic response of brown adipose tissue to cold exposure

Adcyap1 polymorphism covaries with breeding latitude in a Nearctic migratory songbird, the Wilson's warbler (Cardellina pusilla)

Suprachiasmatic Nucleus Neuropeptides and Their Control of Endogenous Glucose Production

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