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Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [array]

ABSTRACT: Late eating has been linked to obesity risk. It is not clear whether this is caused by changes in hunger and appetite, energy expenditure or both, nor what molecular pathways in adipose tissues are involved. We conducted a randomized crossover trial to determine the effects of late vs. early meal schedule on the above measures while rigorously controlling for nutrient intake, fasting duration, light exposure, physical activity and sleep opportunity. Late mealtimes doubled the odds of participants reporting hunger (p<0.0001), increased 24-h ghrelin:leptin ratio (p<0.0001) and decreased waketime energy expenditure (p=0.002). Adipose biopsy directional gene expression analyses showed alterations of several pathways attributed to late mealtimes: TGF-β signaling, lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, and autophagy, indicating decreased lipolysis/increased lipid synthesis, particularly for phospholipids and membrane-bound lipids. These findings may help develop evidence-based approaches for using appropriate meal timing to prevent and/or treat obesity.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190166 | GEO | 2021/12/06

REPOSITORIES: GEO

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Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [RNA-Seq]

Project description:Late eating has been linked to obesity risk. It is not clear whether this is caused by changes in hunger and appetite, energy expenditure or both, nor what molecular pathways in adipose tissues are involved. We conducted a randomized crossover trial to determine the effects of late vs. early meal schedule on the above measures while rigorously controlling for nutrient intake, fasting duration, light exposure, physical activity and sleep opportunity. Late mealtimes doubled the odds of participants reporting hunger (p<0.0001), increased 24-h ghrelin:leptin ratio (p<0.0001) and decreased waketime energy expenditure (p=0.002). Adipose biopsy directional gene expression analyses showed alterations of several pathways attributed to late mealtimes: TGF-β signaling, lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, and autophagy, indicating decreased lipolysis/increased lipid synthesis, particularly for phospholipids and membrane-bound lipids. These findings may help develop evidence-based approaches for using appropriate meal timing to prevent and/or treat obesity.

2021-12-06 | GSE190167 | GEO

Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue

Project description:Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue

| PRJNA786195 | ENA

Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [array]

Project description:Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [array]

| PRJNA786197 | ENA

Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [RNA-Seq]

Project description:Late eating decreases energy expenditure, increases hunger and appetite, and modifies metabolic pathways in adipose tissue [RNA-Seq]

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KDM4B epigenetically protects against obesity and metabolic dysfunction [gene expression]

Project description:KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Mechanistically, we determined that KDM4B directly controls the expression of multiple metabolic genes.

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Four-and-a-half LIM domain protein 2 (FHL2) deficiency protects mice from diet-induced obesity and high FHL2 expression correlates with obesity in man.

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2021-06-14 | GSE156027 | GEO

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Bile acid-induced inflammatory signaling in mice lacking Foxa2 in the liver leads to activation of mTOR and age-onset obesity

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Adipocyte YTH N(6)-methyladenosine RNA-binding protein 1 protects against obesity by promoting white adipose tissue beiging in male mice

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2023-02-02 | GSE197173 | GEO

Targeting parvalbumin promotes M2 macrophage polarization energy expenditure in diet-induced mouse obesity models

Project description:Exercise benefits M2 macrophage polarization, energy homeostasis and protects against obesity partially through exercise-induced circulating factors. Here, by unbiased quantitative proteomics on serum samples from sedentary and exercised mice, we identify parvalbumin as a circulating factor suppressed by exercise. Parvalbumin functions as a non-competitive CSF1R antagonist to inhibit M2 macrophage activation and energy expenditure in adipose tissue. More importantly, serum concentrations of parvalbumin positively correlate with obesity in mouse and human, while treating mice with a recombinant parvalbumin blocker prevents its interaction with CSF1R and promotes M2 macrophage polarization and ameliorates diet-induced obesity. Thus, although further studies are required to assess the significance of parvalbumin in mediating the effects of exercise, our results implicate parvalbumin as a potential therapeutic strategy against obesity.

2022-05-10 | PXD033582 | Pride

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