Central leptin and ghrelin signalling: Comparing and contrasting their mechanisms of action in the brain

Shan, Xiaoye; Yeo, Giles S.H.

doi:10.1007/s11154-011-9171-7

Cited by 23 publications

(23 citation statements)

References 152 publications

(200 reference statements)

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“…Ghrelin and leptin are two hormones that have been recognized to have a major influence on energy balance [32,33]. Previous clinical studies involving SR showed inconsistent results as indicated by others [34,35].…”

Section: Discussionmentioning

confidence: 99%

Influence of sleep restriction on weight loss outcomes associated with caloric restriction

Wang

Sparks

Bowyer

et al. 2018

Sleep

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Study Objectives: To examine the effects of moderate sleep restriction (SR) on body weight, body composition, and metabolic variables in individuals undergoing caloric restriction (CR). Methods:Overweight or obese adults were randomized to an 8 week caloric restriction (CR) regimen alone (n = 15) or combined with sleep restriction (CR + SR) (n = 21). All participants were instructed to restrict daily calorie intake to 95 per cent of their measured resting metabolic rate. Participants in the CR + SR group were also instructed to reduce time in bed on five nights and to sleep ad libitum on the other two nights each week. Results:The CR + SR group reduced sleep by 57 ± 36 min per day during SR days and increased sleep by 59 ± 38 min per day during ad libitum sleep days, resulting in a sleep reduction of 169 ± 75 min per week. The CR and CR + SR groups lost similar amounts of weight, lean mass, and fat mass. However, the proportion of total mass lost as fat was significantly greater (p = 0.016) in the CR group. This proportion was greater than body fat percentage at baseline for the CR (p = 0.0035), but not the CR + SR group. Resting respiratory quotient was reduced (p = 0.033) only in CR, and fasting leptin concentration was reduced only in CR + SR (p = 0.029).Conclusions: Approximately 1 hr of SR on five nights a week led to less proportion of fat mass loss in individuals undergoing hypocaloric weight loss, despite similar weight loss. SR may adversely affect changes in body composition and "catch-up" sleep may not completely reverse it. Clinical trial registration: ClinicalTrials.gov (NCT02413866)Key words: sleep restriction; weight loss; body composition; chronic; caloric restriction Statement of SignificancePrevious studies suggest that sleep restriction during caloric restriction adversely affects weight-loss outcomes. This study extends previous findings by examining the effects of a much longer duration of intervention (8 weeks) using a randomized controlled trial (caloric restriction alone or combined with sleep restriction). Furthermore, the sleep restriction was moderate, approximated 60 min shorter on the 5 days of restricted sleep each week. Ad libitum sleep was allowed on the other 2 days each week so that the sleep pattern mimicked real life. We found that sleep restriction resulted in less loss of fat but greater loss of lean mass among the total mass lost, despite similar weight loss between the two groups. Other metabolic changes were also observed.

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Section: Discussionmentioning

confidence: 99%

Influence of sleep restriction on weight loss outcomes associated with caloric restriction

Wang

Sparks

Bowyer

et al. 2018

Sleep

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“…Also male progeny of dams exposed to HFA only slightly increased the intake of food, to a much lower degree than that observed in females, which was not enough to induce an increase in weight gain, as observed for female progeny of dams exposed to HFA. While the observed hyperleptinemia in male offspring of dams exposed to HFA may represent some degree of leptin resistance, and may eventually predict an increased risk of diabetes (Schmidt et al 2006), it may also exert some anorexigenic effect (Shan & Yeo 2011) and thus protect male offspring from overt hyperphagia and from concomitant excessive weight gain, upon early-life HFA exposure.…”

Section: Discussionmentioning

confidence: 99%

Excess perigestational folic acid exposure induces metabolic dysfunction in post-natal life

Keating¹,

Correia-Branco²,

Araújo³

et al. 2015

Journal of Endocrinology

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The aim of this study was to understand whether high folic acid (HFA) exposure during the perigestational period induces metabolic dysfunction in the offspring, later in life. To do this, female Sprague-Dawley rats (G0) were administered a dose of folic acid (FA) recommended for pregnancy (control, C, 2 mg FA/kg of diet, nZ5) or a high dose of FA (HFA, 40 mg FA/kg of diet, nZ5). Supplementation began at mating and lasted throughout pregnancy and lactation. Body weight and food and fluid intake were monitored in G0 and their offspring (G1) till G1 were 13 months of age. Metabolic blood profiles were assessed in G1 at 3 and 13 months of age (3M and 13M respectively). Both G0 and G1 HFA females had increased body weight gain when compared with controls, particularly 22 (G0) and 10 (G1) weeks after FA supplementation had been stopped. G1 female offspring of HFA mothers had increased glycemia at 3M, and both female and male G1 offspring of HFA mothers had decreased glucose tolerance at 13M, when compared with matched controls. At 13M, G1 female offspring of HFA mothers had increased insulin and decreased adiponectin levels, and G1 male offspring of HFA mothers had increased levels of leptin, when compared with matched controls. In addition, feeding of fructose to adult offspring revealed that perigestational exposure to HFA renders female progeny more susceptible to developing metabolic unbalance upon such a challenge. The results of this work indicate that perigestational HFA exposure the affects long-term metabolic phenotype of the offspring, predisposing them to an insulin-resistant state.

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“…For instance, ghrelin and leptin, secreted from the endocrine cells of the stomach and the adipose tissues, respectively, are transported across the blood-brain barrier, and affect food intake via the hypothalamus. 45 They may also affect neurons in the memory regions of the brain including the hippocampus. 45 The current study presents another example.…”

Section: Discussionmentioning

confidence: 99%

Secreted calmodulin-like skin protein inhibits neuronal death in cell-based Alzheimer’s disease models via the heterotrimeric Humanin receptor

et al. 2013

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Humanin is a secreted bioactive peptide that is protective in a variety of death models, including cell-based neuronal death models related to Alzheimer's disease (AD). To mediate the protective effect in AD-related death models, Humanin signals via a cell-surface receptor that is generally composed of three subunits: ciliary neurotrophic factor receptor α, WSX-1 and gp130 (heterotrimeric Humanin receptor; htHNR). However, the protective effect of Humanin via the htHNR is weak (EC50=1–10 μℳ); therefore, it is possible that another physiological agonist for this receptor exists in vivo. In the current study, calmodulin-like skin protein (CLSP), a calmodulin relative with an undefined function, was shown to be secreted and inhibit neuronal death via the htHNR with an EC50 of 10–100 pℳ. CLSP was highly expressed in the skin, and the concentration in circulating normal human blood was ∼5 nℳ. When administered intraperitoneally in mice, recombinant CLSP was transported across the blood-cerebrospinal fluid (CSF)-barrier and its concentration in the CSF reaches 1/100 of its serum concentration at 1 h after injection. These findings suggest that CLSP is a physiological htHNR agonist.

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Central leptin and ghrelin signalling: Comparing and contrasting their mechanisms of action in the brain

Cited by 23 publications

References 152 publications

Influence of sleep restriction on weight loss outcomes associated with caloric restriction

Influence of sleep restriction on weight loss outcomes associated with caloric restriction

Excess perigestational folic acid exposure induces metabolic dysfunction in post-natal life

Secreted calmodulin-like skin protein inhibits neuronal death in cell-based Alzheimer’s disease models via the heterotrimeric Humanin receptor

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