FGF21 protein
- Known as:
- FGF21 protein
- Catalog number:
- 80R-4397
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- FGF21 protein
Related genes to: FGF21 protein
- Gene:
- FGF21 NIH gene
- Name:
- fibroblast growth factor 21
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2014-11-18
Related products to: FGF21 protein
Related articles to: FGF21 protein
- Oral cholera vaccines (OCVs) show variable immunogenicity in endemic settings. Host factors including enteric dysfunction, systemic inflammation, and nutritional status may influence responses, yet their role in shaping OCV immune responses is not fully understood. This study examined associations between pre-vaccination biomarkers spanning these domains and vibriocidal seroconversion to an OCV, while characterizing how the same biomarker profiles are altered during acute natural infection. - Source: PubMed
Publication date: 2026/08/14
Liswaniso FraserPhiri BernardChibuye MwelwaLuchen Charlie CNgosa DennisNg'ombe HarrietChibesa KennedyMuchimba MutintaChilengi RomaBosomprah SamuelChisenga Caroline C - Dietary protein restriction (PR) is a well-recognized nutritional intervention that enhances metabolic health and extends lifespan. However, the mechanisms behind this phenomenon are not well understood. Here, using genetic loss-of-function models for fibroblast growth factor 21 (Fgf21) and its obligate co-receptor β-Klotho (Klb), we demonstrate that FGF21-KLB signalling in adipocytes is indispensable for the anti-senescence effects of PR. Specifically, adipocyte FGF21 signalling preserves mitochondrial integrity, maintains an anti-inflammatory milieu and sustains nicotinamide adenine dinucleotide (NAD) homeostasis under PR. Mechanistically, FGF21 enhances adipocyte NAD abundance through activation of AMP-activated protein kinase to maintain mitochondrial integrity. Additionally, high-protein feeding induces adipocyte senescence and metabolic dysfunction could be mitigated by exogenous FGF21 supplementation. Together, these findings establish adipose FGF21 signalling as a pivotal endocrine axis that couples dietary protein availability to adipocyte NAD metabolism and identify it as a promising target for the prevention and treatment of age-related metabolic disorders. KEY POINTS: Dietary protein restriction improves metabolic health and extends lifespan, but the mechanisms responsible for these benefits are not fully understood. Fibroblast growth factor 21 (FGF21) is a hormone strongly induced by low-protein diets and has emerged as an important regulator of metabolic adaptation. We show that FGF21 signalling specifically in adipose tissue is essential for the anti-senescence effects of dietary protein restriction. FGF21 preserves mitochondrial integrity by maintaining nicotinamide adenine dinucleotide metabolism through AMP-activated protein kinase activation. Targeting the FGF21-adipose tissue pathway may provide new strategies to prevent or treat age-related metabolic dysfunction. - Source: PubMed
Publication date: 2026/08/28
Yang XiaohanWu YanniYang YiHuang LongJin XianyangJiang XuemeiJin ChaoFeng BinChe LianqiangXu ShengyuLin YanZhuo YongWu DeHua Lun - Nutrition is a fundamental regulator of juvenile development. The persistently high global prevalence of childhood undernutrition and consequent stunting underscores the urgent need to better understand how nutritional status shapes developmental trajectories. Biological sex has recently emerged as a key risk factor for stunting, with boys consistently exhibiting greater vulnerability. This review examines the biological basis of sex differences in physiological adaptation to nutritional stress, focusing specifically on dietary protein deficiency during the juvenile period. Two critical developmental processes display pronounced sexual dimorphism under protein restriction: linear growth and reproductive maturation. Evidence from both preclinical and clinical studies indicates that juvenile protein restriction differentially affects these processes in males and females, highlighting the necessity of considering sex as a biological variable in experimental design and data interpretation. Shared endocrine signals, including Fibroblast Growth Factor 21, may contribute to these sex-specific adaptive responses. Further elucidating the nutritional, endocrine and metabolic mechanisms underlying sexually dimorphic outcomes of juvenile development is essential for enhancing the mechanistic value and translational relevance of preclinical and clinical research. - Source: PubMed
Publication date: 2026/08/28
Joly AmélieLeulier François - Psoriasis is an immune-mediated inflammatory disease accompanied by metabolic syndrome (MetS). FGF-21, leptin, Nrg-4, and hs-CRP may reflect cardiometabolic dysfunction. - Source: PubMed
Publication date: 2026/08/28
Ulutaş Demirbaş GözdeTunçez Akyürek FatmaAkyürek Fikret - An increasing number of patients are being diagnosed with metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD results from disturbances in hepatic lipid metabolism and is associated with an increased risk of cirrhosis and hepatocellular carcinoma and significant extrahepatic morbidity, including cardiovascular disease and malignancies. The pathogenesis of MASLD stems from a multifactorial interaction among genetic susceptibility, epigenetic modifications and environmental factors, which collectively impair systemic metabolic homeostasis. Current management relies on a combination of lifestyle modification and pharmacotherapy. Resmetirom is the first drug registrated for the treatment of adults with MASLD and moderate to advances fibrosis. Over the next decade, multiple promising pharmacotherapies with diverse mechanisms of action and routes of administration are expected to become available for the treatment of MASLD. This narrative review provides an overview of the evolving pharmacological therapeutic landscape for MASLD, with a focus on novel therapeutic agents in late-stage clinical development as THR-β Agonists, GLP-1 Receptor Agonists, Dual GLP-1/ GIP Agonists, Glucagon/GLP-1 Dual Agonists, FGF-21 Analogues, Pan-PPAR Agonists and FASN Inhibitors. Based on the differences in mechanisms of actions and specific side effects of these therapies, the characteristics of patients with MASLD should be taken into account in the decision which pharmacologic treatment should be initiated in an individual patient. Also, combining different therapies could be beneficial since this appears to possess complementary mechanisms. - Source: PubMed
Publication date: 2026/08/27
Straatmijer TessaMulder Midas