&lt;p&gt;Association of Serum Fibroblast Growth Factor 23 Levels with the Presence and Severity of Hepatic Steatosis Is Independent of Sleep Duration in Patients with Diabetes&lt;/p&gt;

Hu, Xiang; Yang, Lijuan; Wang, Yu; Pan, Wei; Chen, Xueqin; Li, Qianqian; Zhou, Jingzong; Gu, Xuejiang

doi:10.2147/dmso.s241348

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…There is a long-standing and well-established relationship of diseases of the kidney, the critical site for phosphate excretion, with elevated serum FGF23 levels. However, increases in FGF23 have more recently also been linked to diseases and their outcomes in a number of organs outside the bone-kidney axis of mineral regulation including liver, lung and heart [ 6 – 8 , 10 , 43 – 45 ]. Whether these organs are a source of FGF23 and/or are responsive to this hormone are unclear.…”

Section: Discussionmentioning

confidence: 99%

“…A prime example of the effects of injury in the liver on other organs is the association of NAFLD with cardiovascular and renal disease [ 22 ]. We have demonstrated Fgf23 induction in a mouse model of NAFLD and increased serum FGF23 levels have been found in human NAFLD [ 7 , 43 ]. Liver-produced FGF23 may therefore have endocrine effects in these extrahepatic diseases.…”

Section: Discussionmentioning

confidence: 99%

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Mouse liver injury induces hepatic macrophage FGF23 production

et al. 2022

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Fibroblast growth factor 23 (FGF23) is a bone marrow cell produced hormone that functions in the intestine and kidney to regulate phosphate homeostasis. Increased serum FGF23 is a well-established predictor of mortality in renal disease, but recent findings linking increased levels to hepatic and cardiac diseases have suggested that other organs are sources of FGF23 or targets of its effects. The potential ability of the liver to produce FGF23 in response to hepatocellular injury was therefore examined. Very low levels of Fgf23 mRNA and FGF23 protein were detected in normal mouse liver, but the amounts increased markedly during acute liver injury from the hepatotoxin carbon tetrachloride. Serum levels of intact FGF23 were elevated during liver injury from carbon tetrachloride. Chronic liver injury induced by a high fat diet or elevated bile acids also increased hepatic FGF23 levels. Stimulation of toll-like receptor (TLR) 4-driven inflammation by gut-derived lipopolysaccharide (LPS) underlies many forms of liver injury, and LPS induced Fgf23 in the liver as well as in other organs. The LPS-inducible cytokines IL-1β and TNF increased hepatic Fgf23 expression as did a TLR2 agonist Pam2CSK3. Analysis of Fgf23 expression and FGF23 secretion in different hepatic cell types involved in liver injury identified the resident liver macrophage or Kupffer cell as a source of hepatic FGF23. LPS and cytokines selectively induced the hormone in these cells but not in hepatocytes or hepatic stellate cells. FGF23 failed to exert any autocrine effect on the inflammatory state of Kupffer cells but did trigger proinflammatory activation of hepatocytes. During liver injury inflammatory factors induce Kupffer cell production of FGF23 that may have a paracrine proinflammatory effect on hepatocytes. Liver-produced FGF23 may have systemic hormonal effects as well that influence diseases in in other organs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mouse liver injury induces hepatic macrophage FGF23 production

et al. 2022

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“…He et al have exhibited a positive correlation of serum FGF23 level with NAFLD and fatty liver index in 331 diabetic inpatients, 17 and Hu et al have found that serum FGF23 level was positively correlated with the presence and severity of NAFLD using Fibro-Scan to evaluate hepatic steatosis in 296 diabetic inpatients. 18 Since the concept of MAFLD was proposed recently, the correlation between serum FGF23 level and MAFLD remains unclear and only inpatients with diabetes have been included in previous studies that examine this association. We selected a large sample of participants (n=1827) from the community and we found that per SD increase in serum FGF23 was associated with a higher risk of MAFLD (19%) after adjusting for age, sex, liver enzymes, and metabolism indices.…”

Section: Discussionmentioning

confidence: 99%

“… 9 , 17 Additionally, FGF23 is proven to be relevant to NAFLD in diabetic patients. 18 , 19 However, the relation of serum FGF23 with MAFLD has not been reported in community population yet. This study aimed to explore the link between serum FGF23 level, MAFLD, and liver fat content (LFC) assessed by standardized ultrasound hepatic/renal ratio and hepatic attenuation rate in a community-based population.…”

Section: Introductionmentioning

confidence: 99%

Serum Fibroblast Growth Factor 23 Level and Liver Fat Content in MAFLD: A Community-Based Cohort

Cao¹,

Xu²,

Shen³

et al. 2021

DMSO

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Purpose Although fibroblast growth factor-23 (FGF23) is involved in the development of metabolic diseases, its association with metabolic-associated fatty liver disease (MAFLD) remains unknown. We explored the relationship between serum fibroblast growth factor-23 level, metabolic associated fatty liver disease, and liver fat content. Patients and Methods Participants were enrolled from communities in Shanghai. Serum fibroblast growth factor-23 level was determined using two-side sandwich enzyme-linked immunosorbent assays. MAFLD was diagnosed using the international expert consensus (2020) criteria. Liver fat content was assessed using ultrasound. Results We enrolled 1827 individuals aged 30–80 years (mean age, 59.4±7.3 years). MAFLD was diagnosed in 445/1393 (31.9%) non-diabetic participants and 245/434 (56.5%) diabetic participants. After adjusting for confounders, one standard deviation increase in serum FGF23 was associated with MAFLD in diabetic (odds ratio, 1.27; 95% confidence interval, 1.15–1.49; P <0.001) and non-diabetic (odds ratio, 1.28; 95% confidence interval, 1.07–1.74; P =0.030) groups. In a fully adjusted linear regression model, serum FGF23 emerged as a positive determinant of liver fat content in both diabetic and non-diabetic groups ( P =0.039; P =0.034). Conclusion Participants with MAFLD had higher serum fibroblast growth factor-23 level than those without MAFLD, regardless of diabetes status. Serum fibroblast growth factor-23 was independently related to MAFLD and liver fat content.

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