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GDF15 reduces NAFLD through mechanisms that are independent of the suppression of food intake

ABSTRACT: The effects of recombinant human GDF15 and matched caloric restriction in pair-fed controls on obesity and NAFLD in mice fed western diet high in both fat and fructose and housed at thermoneutrality (TN, 29 °C).

ORGANISM(S): Mus musculus

PROVIDER: GSE229708 | GEO | 2023/04/14

REPOSITORIES: GEO

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GDF15 Resolves Liver Inflammation in MASH Independently of Reductions in Food Intake or Weight Loss

Project description:Growth differentiation factor 15 (GDF15) is strongly associated with metabolic dysfunction-associated steatohepatitis (MASH), yet whether it drives disease or protects against liver injury remains unresolved. Using thermoneutral mouse models that closely mimic human MASH, we show that loss of GDF15 or its receptor GFRAL selectively worsens hepatic inflammation and fibrosis independently of steatosis or insulin resistance. Conversely, recombinant GDF15 suppressed liver inflammation and fibrosis more effectively than matched caloric restriction despite equivalent reductions in food intake, body weight, and steatosis. Spatial transcriptomics and bulk RNA-seq revealed that GDF15 remodels the hepatic immune-fibrotic niche by suppressing pro-inflammatory macrophages, plasma B cells, and activated stellate cells while promoting pro-resolving immune programs. These effects required GFRAL but occurred independently of β-adrenergic signaling. In a steatosis-free CCl₄ model, GDF15 retained potent anti-inflammatory effects and activated hypothalamic-pituitary-adrenal (HPA) axis and hepatic glucocorticoid receptor (GR) signaling, which were blunted by GR antagonism. Together, these findings identify GDF15 as an endogenous neuroimmune regulator that restrains liver inflammation and fibrosis independently of weight loss or steatosis through a GFRAL–HPA–GR signaling axis.

2026-08-25 | PXD083028 | Pride

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GDF15 increases cAMP/PKA signaling in tibialis anterior (TA) muscle compared to pair-fed controls

Project description:The effects of recombinant human GDF15 on Sympathetic Nervous System (SNS) signalling in skeletal muscle during the caloric restriction in mice.

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GDF15 reduces NAFLD through mechanisms that are independent of the suppression of food intake

Project description:GDF15 reduces NAFLD through mechanisms that are independent of the suppression of food intake

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GDF15 neutralization restores muscle function and physical performance in a mouse model of cancer cachexia

Project description:Cancer cachexia is a disorder characterized by both involuntary weight loss and impaired physical performance. Decline in physical performance of patients with cachexia is associated with poor quality of life, and currently there are no effective pharmacological interventions that restore physical performance. Here we examined the effect of GDF15 neutralization in a mouse model of cancer-induced cachexia (TOV21G) that manifested weight loss and muscle function impairments. With comprehensive assessments, our results demonstrated that cachectic mice treated with the anti-GDF15 antibody mAB2 exhibited body weight gain with near-complete restoration of muscle mass and markedly improved muscle function and physical performance. Mechanistically, the improvements induced by GDF15 neutralization were primarily attributed to increased caloric intake, while altered gene expressions in cachectic muscles were restored in both caloric intake-dependent and -independent manners. The findings implicate the potential of GDF15 neutralization as an effective therapy to enhance physical performance of patients with cachexia.

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GDF15 Suppresses Liver Inflammation Independently of Weight Loss through Neuroendocrine Glucocorticoid Signaling

Project description:Growth differentiation factor 15 (GDF15) is strongly associated with metabolic dysfunction-associated steatohepatitis (MASH), yet whether it promotes or protects against liver injury remains unclear. Using thermoneutral mouse models that closely resemble human MASH, genetic deletion of GDF15 or its receptor GFRAL selectively worsened hepatic inflammation and fibrosis without altering steatosis or insulin resistance. Conversely, recombinant GDF15 reduced liver inflammation and fibrosis more effectively than matched caloric restriction despite identical reductions in food intake, body weight, and steatosis, demonstrating weight loss-independent hepatoprotection. These effects required GFRAL but were independent of β-adrenergic signaling. Instead, GDF15 activated the hypothalamic-pituitary-adrenal (HPA) axis, increasing circulating corticosterone and hepatic glucocorticoid receptor signaling. Spatial transcriptomics and RNA sequencing demonstrated that GDF15 remodeled the hepatic immune-fibrotic niche by suppressing inflammatory macrophages, plasma B cells, and activated stellate cells while promoting pro-resolving immune programs. Together, these findings identify a GDF15-GFRAL-HPA axis that restrains liver inflammation independently of weight loss.

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GDF15 Suppresses Liver Inflammation Independently of Weight Loss through Neuroendocrine Glucocorticoid Signaling

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GDF15 Expression in Thermogenic Adipocytes Regulates Energy Homeostasis in a Sex-dependent Manner

Project description:Diet-induced obesity (DIO) induces growth differentiation factor 15 (GDF15) in various tissues, leading to increased GDF15 serum levels. The liver is the primary source of circulating GDF15 during DIO, but other tissues are also required. We investigated whether brown adipose tissue (BAT) contributes to GDF15 circulating levels and whether Gdf15 induction in BAT regulates systemic metabolism during DIO. We generated mice with selective Gdf15 deletion in thermogenic adipocytes (KO) and subjected them to 12 weeks of high-fat diet (HFD) feeding. Although in ad-libitum fed conditions GDF15 serum levels were unchanged between genotypes regardless of sex, female KO mice demonstrated reduced food intake, increased mitochondrial fatty acid oxidation in BAT, and were resistant to DIO, which was prevented by ovariectomy. Conversely, male KO mice demonstrated increased food intake, reduced mitochondrial respiratory capacity, and increased fibro-inflammation in BAT, resulting in increased body weight and fat mass accrual. Together, our data show that Gdf15 expression in BAT is required to regulate energy metabolism in mice in a sex-dependent manner.

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Effects of fescue toxicosis under chronic heat conditions conditions

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2007-08-14 | GSE8754 | GEO

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