Background: Fibroblast growth factor 19 (FGF19) takes part in maintaining the balance of glycolipids and may be involved in regulating the secretory activity of islet beta cells in patients with type 2 diabetes. This study aimed to evaluate the relationship between the levels of serum FGF19 and endogenous islet beta cell function in type 2 diabetic patients.
Methods: Samples were obtained from 271 subjects: 85 drug-naïve type 2 diabetes participants exclusively on lifestyle intervention (N-DM group), 122 type 2 diabetes subjects previously used medications (DM group) and 64 normal controls (NC group). Serum FGF19 concentrations were measured by ELISA. The insulin sensitivity (MI), insulin secretion (AUC/AUC) and insulin secretion-sensitivity index-2 (ISSI-2) were also measured in the N-DM and DM.
Results: Serum FGF19 levels decreased, in order, from the NC group [median (interquartile range), 245.03 (126.23-317.43) pg/mL] to the N-DM group [170.05 (89.01-244.70) pg/mL] and, finally, to the DM group [142.25 (55.55-187.58) pg/mL] ( for trend < 0.05). Among subjects in the DM group, there was a positive trend in the serum FGF19 concentration; plasma insulin levels at 60 min, 120 min (INS60, INS120, respectively); and area under the insulin curve (AUC) at two points (= 0.214, = 0.025; = 0.189, = 0.048; = 0.188, = 0.049). However, the differences were no longer observed among the N-DM subjects. Simultaneously, the ISSI-2 was closely related to the serum FGF19 levels ( = 0.297, = 0.002) among DM subjects. Furthermore, after adjusting for age, sex, duration, therapy and other clinical factors via multiple logistic regression analysis, ISSI-2 was a key independent factor in the levels of FGF19 (=, =, =).
Conclusions: The serum FGF19 level has a close relation with endogenous beta cell function among DM subjects, as assessed by the ISSI-2. As ISSI-2 is higher in N-DM group, FGF19 may be a main protector in dysfunction of beta cell.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6760053 | PMC |
http://dx.doi.org/10.1186/s13098-019-0475-1 | DOI Listing |
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