scholarly journals Relationship of Serum Fibroblast Growth Factor 21 with Abnormal Glucose Metabolism and Insulin Resistance: The Baltimore Longitudinal Study of Aging

2012 ◽  
Vol 97 (4) ◽  
pp. 1375-1382 ◽  
Author(s):  
Richard D. Semba ◽  
Kai Sun ◽  
Josephine M. Egan ◽  
Candace Crasto ◽  
Olga D. Carlson ◽  
...  

Context: The relationship of fibroblast growth factor 21 (FGF21) with glucose metabolism and insulin resistance has not been well characterized in community-dwelling adults. Objective: The objective of the study was to examine the relationship of FGF21 with glucose metabolism and insulin resistance. Design: Serum FGF21, fasting plasma glucose (FPG), glucose tolerance, and insulin resistance were measured in a cross-sectional study, 2002–2007. Setting: The study was the Baltimore Longitudinal Study of Aging, a natural history cohort study of aging in community-dwelling men and women. Participants: Seven hundred adults, mean age 63.3 yr, participated in the study. Main Outcome Measures: FPG, 2-h plasma glucose, homeostasis model of insulin resistance, whole-body insulin sensitivity (Matsuda index), glucose area under the curve (AUC), and insulin AUC were measured. Results: Overall, the median (25th and 75th percentiles) FGF21 concentration was 225 (126, 370) pg/ml. The proportion of adults with normal, impaired, and diabetic FPG was 77.0, 21.4, and 1.6%, and those with normal, impaired, and diabetic 2-h plasma glucose was 76.7, 19.1, and 4.1%, respectively. Log serum FGF21 (picograms per milliliter), per 1 sd increase, was associated with an FPG (odds ratio 1.43, 95% confidence interval 1.15, 1.77, P = 0.001) and with 2-h plasma glucose (odds ratio 1.39, 95% confidence interval 1.12, 1.73, P = 0.003), in respective multivariate, ordered logistic regression models, adjusted for potential confounders. Serum FGF21 (picograms per milliliter) was associated with the homeostasis model of insulin resistance, the Matsuda index, glucose AUC, and insulin AUC (all P < 0.0001) in respective multivariable linear regression models adjusted for potential confounders. Conclusions: Higher serum FGF21 concentrations were associated with abnormal glucose metabolism and insulin resistance in community-dwelling adults.

2020 ◽  
Author(s):  
Tao Hong ◽  
Jiao-Yang Li ◽  
Ya-Di Wang ◽  
Xiao-Yan Qi ◽  
Zhe-Zhen Liao ◽  
...  

Abstract Objective: Asprosin, a new adipocytokine, has been reported to be related with glucose release, dyslipidemia and insulin resistance (IR). However, the relationship of asprosin with metabolic syndrome (MetS) remains unknown. This study aims to investigate serum asprosin levels in MetS as well as its association with various metabolic parameters in humans.Methods: The consecutive 131 patients with MetS and age-matched 162 healthy subjects were recruited for this study. Serum asprosin concentrations were determined by ELISA. Lipid profile, glucose, insulin, and inflammatory markers were also measured.Results: Serum asprosin levels were higher in subjects with MetS 23.52 (16.70, 32.05) ng/ml compared to 16.70 (12.87, 22.38) ng/ml in the controls (P < 0.01), and showed an increasing trend with the increased numbers of metabolic components (P for trend < 0.01). In all studied subjects, serum asprosin levels were positive correlated with body mass index, waist circumference, percentage of body fat (%), triglyceride, fasting plasma glucose, 2h plasma glucose, fasting insulin, HOMA-IR, interleukin (IL) -6 and monocyte chemoattractant protein (MCP)-1, and negative correlated with HDL cholesterol (P < 0.05). In a multiple linear regression, asprosin was independently and positively correlated with triglyceride and HOMA-IR (P < 0.05). Binary logistic regression revealed that asprosin was independently and positively correlated with the occurrence of MetS and IR even after controlling for anthropometric variables, lipid profiles and inflammatory markers. Conclusion: Asprosin may be a metabolic - related adipokine and related to insulin resistance and MetS. Trial Registration: ChiCTR, ChiCTR1800018347. Registered 12 September 2018, http://www.chictr.org.cn/showproj.aspx?proj=31050.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1812-P
Author(s):  
MARIA D. HURTADO ◽  
J.D. ADAMS ◽  
MARCELLO C. LAURENTI ◽  
CHIARA DALLA MAN ◽  
CLAUDIO COBELLI ◽  
...  

2011 ◽  
Vol 31 (5) ◽  
pp. 1208-1214 ◽  
Author(s):  
Sander J. Robins ◽  
Asya Lyass ◽  
Justin P. Zachariah ◽  
Joseph M. Massaro ◽  
Ramachandran S. Vasan

2009 ◽  
Vol 66 (3) ◽  
pp. 346-349 ◽  
Author(s):  
Elvira Verduci ◽  
Silvia Scaglioni ◽  
Carlo Agostoni ◽  
Giovanni Radaelli ◽  
Marialuisa Biondi ◽  
...  

2014 ◽  
Vol 35 (1) ◽  
pp. 26-40 ◽  
Author(s):  
Ahmed Lawan ◽  
Lei Zhang ◽  
Florian Gatzke ◽  
Kisuk Min ◽  
Michael J. Jurczak ◽  
...  

The liver plays a critical role in glucose metabolism and communicates with peripheral tissues to maintain energy homeostasis. Obesity and insulin resistance are highly associated with nonalcoholic fatty liver disease (NAFLD). However, the precise molecular details of NAFLD remain incomplete. The p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) regulate liver metabolism. However, the physiological contribution of MAPK phosphatase 1 (MKP-1) as a nuclear antagonist of both p38 MAPK and JNK in the liver is unknown. Here we show that hepatic MKP-1 becomes overexpressed following high-fat feeding. Liver-specific deletion of MKP-1 enhances gluconeogenesis and causes hepatic insulin resistance in chow-fed mice while selectively conferring protection from hepatosteatosis upon high-fat feeding. Further, hepatic MKP-1 regulates both interleukin-6 (IL-6) and fibroblast growth factor 21 (FGF21). Mice lacking hepatic MKP-1 exhibit reduced circulating IL-6 and FGF21 levels that were associated with impaired skeletal muscle mitochondrial oxidation and susceptibility to diet-induced obesity. Hence, hepatic MKP-1 serves as a selective regulator of MAPK-dependent signals that contributes to the maintenance of glucose homeostasis and peripheral tissue energy balance. These results also demonstrate that hepatic MKP-1 overexpression in obesity is causally linked to the promotion of hepatosteatosis.


2018 ◽  
Vol 15 (3) ◽  
pp. 14-20
Author(s):  
Yassine Chahirou ◽  
Abdelhalim Mesfioui ◽  
Ali Ouichou ◽  
Aboubaker Hessni

Current studies show that metabolic and behavioral disorders represent severe health problems. Several questions arise about the molecular relationship of metabolic and behavioral disorders. This review will discuss the relationship of lipid metabolism and fructose consumption accompanied by an increase in weight as well as associated disorders: hypertension, insulin-resistance, oxidative stress and depression. Adipose tissue is considered as an endocrine tissue with intense secretory activities (metabolic and inflammatory). These adipokines are responsible for an alteration of several physiological functions. In this review we will try to understand how lipogenesis that causes dyslipidemia can influence insulin resistance, hypertension, oxidative stress, depression and the relationship between these various disorders.


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