Meal Anticipatory Rise in Acylated Ghrelin at Dark Onset is Blunted After Long-Term Fasting in Rats

Zizzari, Philippe; Hassouna, Rim; Longchamps, Romaine; Epelbaum, Jacques; Tolle, Virginie

doi:10.1111/j.1365-2826.2011.02183.x

Cited by 12 publications

(9 citation statements)

References 54 publications

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“…Corticosterone in this group was elevated at ZT0 and ZT4 compared to the ZT16 group, and slightly decreased at ZT12. This pattern conforms to previous reports that in daytime fed rats, corticosterone rises in anticipation of the daytime meal, but also shows a nocturnal peak, reflecting a continued influence of the LD entrained SCN pacemaker [36] .…”

Section: Resultssupporting

confidence: 92%

Circadian Mechanisms of Food Anticipatory Rhythms in Rats Fed Once or Twice Daily: Clock Gene and Endocrine Correlates

et al. 2014

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Circadian clocks in many brain regions and peripheral tissues are entrained by the daily rhythm of food intake. Clocks in one or more of these locations generate a daily rhythm of locomotor activity that anticipates a regular mealtime. Rats and mice can also anticipate two daily meals. Whether this involves 1 or 2 circadian clocks is unknown. To gain insight into how the circadian system adjusts to 2 daily mealtimes, male rats in a 12∶12 light-dark cycle were fed a 2 h meal either 4 h after lights-on or 4 h after lights-off, or a 1 h meal at both times. After 30 days, brain, blood, adrenal and stomach tissue were collected at 6 time points. Multiple clock genes from adrenals and stomachs were assayed by RT-PCR. Blood was assayed for corticosterone and ghrelin. Bmal1 expression was quantified in 14 brain regions by in situ hybridization. Clock gene rhythms in adrenal and stomach from day-fed rats oscillated in antiphase with the rhythms in night-fed rats, and at an intermediate phase in rats fed twice daily. Corticosterone and ghrelin in 1-meal rats peaked at or prior to the expected mealtime. In 2-meal rats, corticosterone peaked only prior the nighttime meal, while ghrelin peaked prior to the daytime meal and then remained elevated. The olfactory bulb, nucleus accumbens, dorsal striatum, cerebellum and arcuate nucleus exhibited significant daily rhythms of Bmal1 in the night-fed groups that were approximately in antiphase in the day-fed groups, and at intermediate levels (arrhythmic) in rats anticipating 2 daily meals. The dissociations between anticipatory activity and the peripheral clocks and hormones in rats anticipating 2 daily meals argue against a role for these signals in the timing of behavioral rhythms. The absence of rhythmicity at the tissue level in brain regions from rats anticipating 2 daily meals support behavioral evidence that circadian clock cells in these tissues may reorganize into two populations coupled to different meals.

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Section: Resultssupporting

confidence: 92%

Circadian Mechanisms of Food Anticipatory Rhythms in Rats Fed Once or Twice Daily: Clock Gene and Endocrine Correlates

et al. 2014

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“…Furthermore, using electrophysiological recording, we have shown that ghrelin‐induced activation of NPY neurones is abolished in GHS‐R null mice . Interestingly, ghrelin has been demonstrated to exhibit daily rhythms of secretion that are synchronised by meal timing in both humans and rodents, showing pre‐prandial increases in circulating acyl‐ghrelin levels in anticipation of scheduled meals . Furthermore, transcriptomic studies have identified GHS‐R as one of the top G‐protein coupled receptors to be significantly up‐regulated by food deprivation compared to fed state in isolated AgRP neurones .…”

Section: Introductionmentioning

confidence: 94%

Ghrelin receptor in agouti‐related peptide neurones regulates metabolic adaptation to calorie restriction

Bongmba

Lee

et al. 2019

J Neuroendocrinology

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Ghrelin is a gut hormone that signals to the hypothalamus to stimulate growth hormone release, increase food intake and promote fat deposition. The ghrelin receptor, also known as growth hormone secretagogue receptor (GHS‐R), is highly expressed in the brain, with the highest expression in agouti‐related peptide (AgRP) neurones in the hypothalamus. Compelling evidence indicates that ghrelin serves as a survival hormone with respect to maintaining blood glucose and body weight during nutritional deficiencies. Recent studies have demonstrated that AgRP neurones are involved in metabolic and behavioural adaptation to an energy deficit to improve survival. In the present study, we used a neuronal subtype‐specific GHS‐R knockout mouse (AgRP‐Cre;Ghsrf/f) to investigate the role of GHS‐R in hypothalamic AgRP neurones in metabolic and behavioural adaptation to hypocaloric restricted feeding. We subjected the mice to a restricted feeding regimen of 40% mild calorie restriction (CR), with one‐quarter of food allotment given in the beginning of the light cycle and three‐quarters given at the beginning of the dark cycle, to mimic normal mouse intake pattern. The CR‐fed AgRP‐Cre;Ghsrf/f mice exhibited reductions in body weight, fat mass and blood glucose. Metabolic profiling of these CR‐fed AgRP‐Cre;Ghsrf/f mice showed a trend toward reduced basal metabolic rate, significantly reduced core body temperature and a decreased expression of thermogenic genes in brown adipose tissue. This suggests a metabolic reset to a lower threshold. Significantly increased physical activity, a trend toward increased food anticipatory behaviour and altered fuel preferences were also observed in these mice. In addition, these CR‐fed AgRP‐Cre;Ghsrf/f mice exhibited a decreased counter‐regulatory response, showing impaired hepatic glucose production. Lastly, hypothalamic gene expression in AgRP‐Cre;Ghsrf/f mice revealed increased AgRP expression and a decreased expression of genes in β‐oxidation pathways. In summary, our data suggest that GHS‐R in AgRP neurones is a key component of the neurocircuitry involved in metabolic adaptation to calorie restriction.

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“…Ghrelin is perhaps best known as a circulating hunger signal necessary for meal initiation and meal anticipation with a secretion occurring in a pulsatile manner starting with a preprandial rise and postprandial fall 1 h after food intake (Ariyasu et al, 2001; Cummings et al, 2001; Tschöp et al, 2001; Zizzari et al, 2011; Merkestein et al, 2012). Moreover, whatever the route of injection, ghrelin increases food intake both in humans and animals (Wren et al, 2001a,b).…”

Section: Ghrelin a Key Energy Balance Hormone: Role In Anorexia Nervosamentioning

confidence: 99%

Ghrelin: Central and Peripheral Implications in Anorexia Nervosa

Méquinion¹,

Langlet²,

Zgheib³

et al. 2013

Front. Endocrinol.

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Increasing clinical and therapeutic interest in the neurobiology of eating disorders reflects their dramatic impact on health. Chronic food restriction resulting in severe weight loss is a major symptom described in restrictive anorexia nervosa (AN) patients, and they also suffer from metabolic disturbances, infertility, osteopenia, and osteoporosis. Restrictive AN, mostly observed in young women, is the third largest cause of chronic illness in teenagers of industrialized countries. From a neurobiological perspective, AN-linked behaviors can be considered an adaptation that permits the endurance of reduced energy supply, involving central and/or peripheral reprograming. The severe weight loss observed in AN patients is accompanied by significant changes in hormones involved in energy balance, feeding behavior, and bone formation, all of which can be replicated in animals models. Increasing evidence suggests that AN could be an addictive behavior disorder, potentially linking defects in the reward mechanism with suppressed food intake, heightened physical activity, and mood disorder. Surprisingly, the plasma levels of ghrelin, an orexigenic hormone that drives food-motivated behavior, are increased. This increase in plasma ghrelin levels seems paradoxical in light of the restrained eating adopted by AN patients, and may rather result from an adaptation to the disease. The aim of this review is to describe the role played by ghrelin in AN focusing on its central vs. peripheral actions. In AN patients and in rodent AN models, chronic food restriction induces profound alterations in the « ghrelin » signaling that leads to the development of inappropriate behaviors like hyperactivity or addiction to food starvation and therefore a greater depletion in energy reserves. The question of a transient insensitivity to ghrelin and/or a potential metabolic reprograming is discussed in regard of new clinical treatments currently investigated.

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Meal Anticipatory Rise in Acylated Ghrelin at Dark Onset is Blunted After Long-Term Fasting in Rats

Cited by 12 publications

References 54 publications

Circadian Mechanisms of Food Anticipatory Rhythms in Rats Fed Once or Twice Daily: Clock Gene and Endocrine Correlates

Circadian Mechanisms of Food Anticipatory Rhythms in Rats Fed Once or Twice Daily: Clock Gene and Endocrine Correlates

Ghrelin receptor in agouti‐related peptide neurones regulates metabolic adaptation to calorie restriction

Ghrelin: Central and Peripheral Implications in Anorexia Nervosa

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