Leptin and brain–adipose crosstalks

Caron, Alexandre; Lee, Syann; Elmquist, Joel K.; Gautron, Laurent

doi:10.1038/nrn.2018.7

Cited by 196 publications

(174 citation statements)

References 217 publications

(274 reference statements)

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“…Evidence from rodent models has shown that leptin influences the programming of hypothalamic circuits during gestation, which may influence ex utero energy metabolism through satiety and hunger signaling . Additionally, leptin may increase brown adipose tissue deposition and enhance the activity of thermoregulatory circuits, which may in turn influence adipose tissue metabolism and deposition during infancy and childhood .…”

Section: Discussionmentioning

confidence: 99%

Neonatal Adipocytokines and Longitudinal Patterns of Childhood Growth

Buck

Eliot

Kelsey

et al. 2019

Obesity

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Objective Adipocytokines are markers of fetal metabolism, but their association with childhood growth is unclear. This study examined associations of neonatal adipocytokines with longitudinal childhood adiposity measures in a prospective cohort of pregnant women and their children. Methods We measured leptin and adiponectin concentrations at delivery and children’s body mass index (BMI) z-scores between ages 4 weeks and 8 years. We estimated differences in BMI z-scores and rates of BMI z-score change by leptin (N = 257) and adiponectin (N = 271) terciles. Results Children in the middle (mean difference: 0.2; 95% CI: −0.1, 0.4) and highest (0.4; 95% CI: 0.1, 0.6) leptin terciles had greater BMI z-scores than children in the lowest tercile. Associations were null after adjustment for birthweight z-score. Children in the lowest adiponectin tercile had greater gains in BMI z-score (change per year: 0.10; 95% CI: 0.08, 0.13) than children in the middle (0.07; 95% CI: 0.04, 0.09) and highest terciles (0.04; 95% CI: −0.01, 0.05) (adiponectin x age interaction P < 0.001). Conclusions Lower adiponectin levels were associated with increased rates of BMI gains in the first 8 years of life. While leptin was positively associated with BMI, this association may be confounded by birthweight.

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Section: Discussionmentioning

confidence: 99%

Neonatal Adipocytokines and Longitudinal Patterns of Childhood Growth

Buck

Eliot

Kelsey

et al. 2019

Obesity

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“…In mice, fasting-induced glycogen shortage activates a liver-brain-adipose neurocircuitry to facilitate fat utilization [61], and the regulation of food intake and glucose homeostasis by liver glycogen is dependent on the hepatic branch of the vagus nerve [62]. In addition, leptin mediated interactions between the brain and adipose depots related to the maintenance of systemic energy balance were recently reviewed [63]. These previous studies provide additional lines of evidence for the existence of our proposed brain-liverfats organ network in the context of STF.…”

Section: A Brain-liver-fats Organ Network Modulated By Stfmentioning

confidence: 99%

Differential regulation of the immune system in a brain-liver-fats organ network during short term fasting

Huang

Makhlouf

AbouMoussa

et al. 2020

Preprint

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Different fasting regiments are known to promote health, and chronic immunological disorders and mitigate age-related pathophysiological parameters in animals and humans. Indeed, several clinicals trials are currently ongoing using fasting as a potential therapy for a wide range of conditions. Fasting alters metabolism by acting as a reset for energy homeostasis, but the molecular mechanisms underlying the beneficial effects of short-term fasting (STF) are still not-well understood, particularly at a systems/multiorgan level. We investigated the dynamic gene expression patterns associated with periods of STF in nine different mouse organs. First, we identified both unique and shared transcriptional signatures at the organ and systemic levels. Second, we discovered differential temporal effects of STF among organs. Third, using gene ontology enrichment analysis, we identified an organ network, formed by the 63 common biological pathways perturbed by STF. This network incorporates the brain, liver, interscapular brown, and perigonadal white adipose tissue, hence we name it the brain-liver-fats organ network. Fourth, we identified that the immune system, dominated by T cell regulation processes, is a central and prominent target of systemic modulations during short-term energy loss in this organ network. The changes we identified in specific immune components point to the priming of adaptive immunity and parallel the fine-tuning of innate immune signaling. In conclusion, our study provides a comprehensive multi-organ transcriptomic profiling of mice subjected to multiple periods of STF and added new insights into the molecular modulators involved in the systemic immuno-transcriptomic changes that occur during short-term energy loss.

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“…These neurons respond to an inflow of peripheral signals, arriving from adipose tissue (including leptin and adiponectin), pancreas (insulin), gut hormones (peptide YY, cholecystokinin, glucagon‐like peptide I, and ghrelin), circulating nutrients (glucose and fatty acids), communicating information regarding the energy status of an organism, which is subsequently translated to a specific response. Both orexigenic and anorexigenic neuron types harbor receptors or sensors for circulating hormones and nutrients …”

Section: Introductionmentioning

confidence: 99%

Both NPY-Expressing and CART-Expressing Neurons Increase Energy Expenditure and Trabecular Bone Mass in Response to AP1 Antagonism, But Have Opposite Effects on Bone Resorption

Idelevich

Sato

Avihai

et al. 2020

Journal of Bone and Mineral Research

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Energy metabolism and bone homeostasis share several neuronal regulatory pathways. Within the ventral hypothalamus (VHT), the orexigenic neurons co‐express Agouti‐related peptide (AgRP) and neuropeptide Y (NPY) and the anorexigenic neurons co‐express, α‐melanocyte stimulating hormone derived from proopiomelanocortin (POMC), and cocaine and amphetamine‐regulated transcript (CART). These neurons regulate both processes, yet their relative contribution is unknown. Previously, using genetically targeted activator protein (AP1) alterations as a tool, we showed in adult mice that AgRP or POMC neurons are capable of inducing whole‐body energy catabolism and bone accrual, with different effects on bone resorption. Here, we investigated whether co‐residing neurons exert similar regulatory effects. We show that AP1 antagonists targeted to NPY‐producing or CART‐producing neurons in adult mice stimulate energy expenditure, reduce body weight gain and adiposity and promote trabecular bone formation and mass, yet again via different effects on bone resorption, as measured by serum level of carboxy‐terminal collagen type I crosslinks (CTX). In addition, AP1 antagonists promote neurite expansion, increasing neurite number, length, and surface area in primary hypothalamic neuronal cultures. Overall, our data demonstrate that the orexigenic NPY and anorexigenic CART neurons both have the capacity to stimulate energy burning state and increase bone mass. © 2020 American Society for Bone and Mineral Research.

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Leptin and brain–adipose crosstalks

Cited by 196 publications

References 217 publications

Neonatal Adipocytokines and Longitudinal Patterns of Childhood Growth

Neonatal Adipocytokines and Longitudinal Patterns of Childhood Growth

Differential regulation of the immune system in a brain-liver-fats organ network during short term fasting

Both NPY-Expressing and CART-Expressing Neurons Increase Energy Expenditure and Trabecular Bone Mass in Response to AP1 Antagonism, But Have Opposite Effects on Bone Resorption

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