scholarly journals Serum Soluble Epidermal Growth Factor Receptor Level Increase in Patients Newly Diagnosed with Type 2 Diabetes Mellitus

2018 ◽  
Vol 42 (4) ◽  
pp. 343 ◽  
Author(s):  
Ji Min Kim ◽  
Sorim Choung ◽  
Kyong Hye Joung ◽  
Ju Hee Lee ◽  
Hyun Jin Kim ◽  
...  
2011 ◽  
Vol 57 (4) ◽  
pp. 32-36
Author(s):  
L A Kuznetsova ◽  
S A Plesneva ◽  
O V Chistiakova ◽  
T S Sharova ◽  
M N Pertseva

This study showed for the first time the stimulating action of peptides of the insulin family, insulin-like growth factor-1, relaxin, and epidermal growth factor (EGF) on the activity of the adenilate cyclase signal system (ACSS) in lymphocytes from the subjects of the control group. These hormonal effects were enhanced in the presence of guanylimidodiphosphate (GIDP). Moreover, leptin was for the first time shown to increase adenilate cyclase activity in lymphocytes from the control subjects and inhibition of this action by antibodies against leptin receptors. The patients presenting with type 2 diabetes mellitus (DM2) showed the enhanced baseline activity of adenilate cyclase in their lymphocytes whereas its stimulation by the above hormones, both in the presence and absence of GIDP, sharply declined. The influence of leptin on adenilate cyclase activity in patients with DM2 was apparent only at its concentrations above 10–8 M; it was inhibited by antibodies to leptin receptors. The results of this study indicate that disturbances of hormonal stimulation of adenilate cyclase activity in lymphocites of diabetic patients may be due to functional defects located at the receptor level in the case of leptin and at the level of Gs protein and its coupling to adenulate cyclase in case of peptides of the insulin family and GF. These findings confirm the concept being developed by the author according to which molecular defects in the hormone-dependent ACSS system constitute one of the main causes underlying the development of DM2.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jacqueline A. Bonds ◽  
Aashutosh Shetti ◽  
Terilyn K. L. Stephen ◽  
Marcelo G. Bonini ◽  
Richard D. Minshall ◽  
...  

Abstract Hippocampal neurogenesis plays an important role in learning and memory function throughout life. Declines in this process have been observed in both aging and Alzheimer’s disease (AD). Type 2 Diabetes mellitus (T2DM) is a disorder characterized by insulin resistance and impaired glucose metabolism. T2DM often results in cognitive decline in adults, and significantly increases the risk of AD development. The pathways underlying T2DM-induced cognitive deficits are not known. Some studies suggest that alterations in hippocampal neurogenesis may contribute to cognitive deterioration, however, the fate of neurogenesis in these studies is highly controversial. To address this problem, we utilized two models of T2DM: (1) obesity-independent MKR transgenic mice expressing a mutated form of the human insulin-like growth factor 1 receptor (IGF-1R) in skeletal muscle, and (2) Obesity-dependent db/db mice harboring a mutation in the leptin receptor. Our results show that both models of T2DM display compromised hippocampal neurogenesis. We show that the number of new neurons in the hippocampus of these mice is reduced. Clone formation capacity of neural progenitor cells isolated from the db/db mice is deficient. Expression of insulin receptor and epidermal growth factor receptor was reduced in hippocampal neurospheres isolated from db/db mice. Results from this study warrant further investigation into the mechanisms underlying decreased neurogenesis in T2DM and its link to the cognitive decline observed in this disorder.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yi Sun ◽  
Minxia Zhu ◽  
Hui Zhao ◽  
Xiaoqing Ni ◽  
Renan Chang ◽  
...  

Purpose. Type 2 diabetes mellitus (T2DM) carries a high risk of hepatocellular carcinoma (HCC). Both serum fibroblast growth factor 19 (FGF19) and bile acid concentrations are associated with T2DM and HCC. We aimed at evaluating the relationships between FGF19 and bile acid concentrations and HCC in patients with T2DM. Methods. Twenty-seven healthy volunteers (control group), 27 patients with T2DM (T2DM group), 16 patients with newly diagnosed HCC (HCC group), and 10 T2DM patients with newly diagnosed HCC (T2DM-HCC group) were studied at the Affiliated Hospital of Nantong University between June 2016 and June 2017. The serum concentrations of serum FGF19 and total bile acids (TBA) were measured in all the participants. Correlation analysis and multiple stepwise regression analysis of the FGF19 and TBA concentrations were performed in all the participants and in the four groups. Results. The concentrations of FGF19 were 220.5 pg/ml, 185.1 pg/ml, 115.8 pg/ml, and 70.4 pg/ml in the HCC, T2DM-HCC, control, and T2DM groups, respectively (p<0.001), and the TBA concentrations were 21.75 μmol/l, 14.25 μmol/l, 3.6 μmol/l, and 3.1 μmol/l (p<0.001). There were positive correlations between the FGF19 and TBA concentrations across all the participants (r = 0.777; p<0.001), and in the control (r = 0.400; p=0.039), T2DM (r = 0.477; p=0.012), HCC (r = 0.684; p=0.003), and T2DM-HCC (r = 0.673; p=0.033) groups. Conclusions. Simultaneous increase of serum FGF19 and TBA levels may be used as indicators of HCC screening at early stage in patients with T2DM.


Sign in / Sign up

Export Citation Format

Share Document