ArticleDiabetologia2024
Postprandial fatty acid-binding protein 4 is associated with muscle insulin resistance.
Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Fasting serum annexin A2 is associated with peripheral insulin sensitivity and may enhance glucose uptake via Src-dependent signaling.Journal of diabetes investigation · 2026Article
- Circulating adipocyte fatty acid-binding protein exacerbates LPS-induced neurotoxicity by crossing the disrupted blood-brain barrier and promoting neuronal apoptosis.Cell communication and signaling : CCS · 2026Article
- Administration of heat killed Fructobacillus fructosus OS-1010 attenuates metabolic disease induced by high fat diet in mice.Scientific reports · 2025Article
- FABP4 as a Mediator of Lipid Metabolism and Pregnant Uterine Dysfunction in Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
aims/hypothesisFatty acid-binding protein 4 (FABP4) has been reported to act as a hepatic insulin resistance factor. We previously reported that fasting FABP4 was correlated with insulin resistance measurements derived from the glucose clamp, and another study reported that postprandial FABP4 levels were decreased in healthy volunteers but were not reported (or known) in participants with type 2 diabetes. We have limited knowledge about the direct effect of FABP4 on muscle cells. We investigated the postprandial FABP4 levels in participants with type 2 diabetes, and the basic mechanism of muscle insulin resistance and FABP4.
methodsWe performed a meal tolerance test and hyperinsulinaemic-euglycaemic clamp in 22 participants with type 2 diabetes and 26 participants without diabetes. We measured fasting and postprandial serum FABP4. We cultured mouse C2C12 muscle cells, and investigated the effect of FABP4 on glucose uptake. We analysed insulin signalling by western blot and insulin binding assay.
resultsThe postprandial FABP4 level in participants with type 2 diabetes was higher than that in participants without diabetes. Participants without diabetes had lower postprandial FABP4 than fasting except for one participant, whereas one-third of participants with type 2 diabetes had higher postprandial FABP4 than fasting. Postprandial FABP4 was correlated with the muscle insulin resistance M/I value from a glucose clamp in participants without diabetes (r=-0.42, p<0.05). The increase in FABP4 after a meal correlated with the muscle insulin resistance M/I value (r=-0.44, p<0.05) and the difference between fasting and postprandial glucagon in participants with type 2 diabetes (r=0.36, p<0.05). FABP4 alone appears to increase glucose uptake, and the combination of FABP4 and insulin decreases glucose uptake when compared with insulin alone. FABP4 inhibits insulin signalling of muscle cells through decreases in phosphorylation of insulin receptor substrate 1 and Akt. The physiological concentration of FABP4 did not inhibit insulin binding to muscle cells. CONCLUSIONS/
interpretationThese results suggested that the postprandial FABP4 level is associated with insulin resistance, and FABP4 may suppress insulin signals.
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