All articles tagged with #fgf21
A Nature Communications study of about 200 Orthodox Christians who regularly fast from meat and dairy, plus a non-fasting control group, shows that short-term animal-product restriction can alter gene expression and metabolic markers—including FGF21—with signs of adipose tissue beiging and a genotype-linked change in the LBR gene, highlighting a complex diet–genetics relationship and the need for further research.
A Cell Press Blue review of over 350 studies finds that restricting protein intake—without cutting total calories—may boost metabolism and cellular maintenance via the FGF21 hormone, offering a potential path to longer, healthier lives for sedentary adults. Active individuals still need protein for muscle, and the review cannot prove causation in humans; long-term, tailored protein guidelines by age and activity level are needed.
A scientific review of 350+ studies suggests that lowering protein intake, rather than calories, can improve metabolism, reduce inflammation, and trigger the hormone FGF21 to boost energy expenditure—potentially extending lifespan in sedentary adults. The review notes benefits for metabolism and cellular maintenance but emphasizes it is not a causal human trial and protein needs should be tailored to age and activity; active individuals still require sufficient protein. More long-term human studies are needed.
A review of 300 studies suggests that lowering protein intake may promote healthier aging by improving metabolism and triggering autophagy via the hormone FGF21, though protein restriction isn’t suitable for everyone (pregnant women, children, the elderly, and those recovering from injury). Official guidelines vary, and researchers advocate personalized protein targets based on activity levels.
A review of more than 350 studies suggests lowering protein intake may improve metabolic health and possibly extend lifespan, especially for sedentary adults. Updated U.S. guidelines now recommend 1.2–1.6 g/kg body weight, up from 0.8 g/kg. The hormone FGF21 rises with lower protein and may help convert white fat to energy-burning beige fat, improving glucose control and reducing inflammation. Active individuals may be protected by exercise, which directs amino acids to muscle growth, but experts say more high-quality human studies are needed to confirm these findings.
A review of more than 350 studies finds that eating less protein can improve metabolic function, reduce inflammation and cellular damage, and activate pathways linked to healthier aging and longer life, especially for sedentary adults who may consume more protein than they actually need. While protein supports muscle with exercise, higher intake isn’t universally beneficial, and certain amino acids (like methionine, isoleucine, and valine) may drive aging when consumed in excess. The hormone FGF21 rises when protein is restricted and is thought to aid energy expenditure and glucose regulation. Protein needs vary by age and activity, suggesting personalized guidelines rather than a one-size-fits-all approach. The findings complement existing ideas about calorie restriction and highlight the importance of tailoring protein intake to individual lifestyles.
A comprehensive review of 350+ studies links lower protein intake to healthier aging and possible lifespan extension by boosting metabolism and the hormone FGF21; amino acids such as methionine, isoleucine, and valine may drive these effects, though protein remains essential for muscle and certain groups, suggesting more personalized protein guidelines rather than a universal high-protein approach.
A broad review of 350+ studies suggests that for many adults, eating less protein could support healthier aging by raising energy expenditure through the FGF21 hormone and altering cell-growth signals; the traditional 0.8 g/kg/day baseline may suffice for sedentary individuals, but needs vary with age, activity, and health, and the findings come with limits since many studies are animal-based.
A study identifies a specific hindbrain neuron population (NTS-KLB) that directly responds to the liver hormone FGF21 to orchestrate changes in food intake, food choice, and energy expenditure during dietary protein restriction, challenging the idea that metabolism is controlled mainly by the hypothalamus and suggesting targeted brain circuits could improve FGF21-based obesity and diabetes therapies.
University of Oklahoma researchers identify FGF21 as a hormone that signals the hindbrain—the same region GLP-1 obesity drugs target—potentially increasing metabolic rate and promoting weight loss in mice. While promising, the findings are preclinical, and safety concerns (digestive issues, bone loss) and human relevance remain unresolved; future therapies may pair FGF21 pathways to treat obesity and related fatty liver disease (MASH).
Researchers found that the hormone FGF21 acts in the hindbrain (nucleus of the solitary tract and area postrema) to regulate metabolism and reduce body weight, signaling a shared yet distinct pathway from GLP-1 drugs. The work, published in Cell Reports, suggests a specific brain circuit could be targeted for obesity and MASH therapies, though current FGF21 analogs can cause GI issues and bone loss, prompting hopes for safer, more precise treatments.
Low-protein diets reshape the gut microbiota to drive white adipose tissue browning through two non-redundant pathways: microbiota-derived bile acids activate FXR in adipose progenitors, while microbial ammonia triggers hepatic FGF21 production; together these signals promote browning and sympathetic innervation. This effect is microbiota-dependent, reversible, and transferable to germ-free mice via defined bacterial consortia that require both ammonia production and bile-acid modification. In humans, FDG-PET–positive browning signals linked to specific microbes can induce browning in mice on an LPD, with four key hu4 strains identified as essential. Inhibiting microbial ammonia production or FXR/FGF21 pathways blocks browning, highlighting a diet–microbiota–host axis shaping adipose remodeling and metabolic responses.
89bio's Phase IIb data showed its drug, an analog of FGF21, was better than placebo at lessening fibrosis without worsening NASH in two of three dose groups. The data pave the way for a potential Phase III, following in the footsteps of another biotech in its drug class, Akero Therapeutics. To fund a late-stage study, 89bio "would need to raise additional capital," with the company having about $188 million at the end of last year.
Researchers have discovered that the hormone fibroblast growth factor 21 (FGF21) can counteract the effects of intoxication in mice, increasing alertness in the brain and fighting against certain effects of drunkenness without fundamentally changing how alcohol is broken down in the body. The liver produces the hormone in both mice and humans, suggesting these results could apply to us, too. The hormone could be used to rouse people suffering from alcohol poisoning or extreme drunkenness so that they could be better treated. Further research is needed to demonstrate these effects in humans.