Soy Leaf Extract Containing Kaempferol Glycosides and Pheophorbides Improves Glucose Homeostasis by Enhancing Pancreatic β-Cell Function and Suppressing Hepatic Lipid Accumulation in db/db Mice

2015 ◽  
Vol 63 (32) ◽  
pp. 7198-7210 ◽  
Author(s):  
Hua Li ◽  
Hyeon-Seon Ji ◽  
Ji-Hyun Kang ◽  
Dong-Ha Shin ◽  
Ho-Yong Park ◽  
...  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Frank Chenfei Ning ◽  
Nina Jensen ◽  
Jiarui Mi ◽  
William Lindström ◽  
Mirela Balan ◽  
...  

AbstractType 2 diabetes mellitus (T2DM) affects millions of people and is linked with obesity and lipid accumulation in peripheral tissues. Increased lipid handling and lipotoxicity in insulin producing β-cells may contribute to β-cell dysfunction in T2DM. The vascular endothelial growth factor (VEGF)-B regulates uptake and transcytosis of long-chain fatty acids over the endothelium to tissues such as heart and skeletal muscle. Systemic inhibition of VEGF-B signaling prevents tissue lipid accumulation, improves insulin sensitivity and glucose tolerance, as well as reduces pancreatic islet triglyceride content, under T2DM conditions. To date, the role of local VEGF-B signaling in pancreatic islet physiology and in the regulation of fatty acid trans-endothelial transport in pancreatic islet is unknown. To address these questions, we have generated a mouse strain where VEGF-B is selectively depleted in β-cells, and assessed glucose homeostasis, β-cell function and islet lipid content under both normal and high-fat diet feeding conditions. We found that Vegfb was ubiquitously expressed throughout the pancreas, and that β-cell Vegfb deletion resulted in increased insulin gene expression. However, glucose homeostasis and islet lipid uptake remained unaffected by β-cell VEGF-B deficiency.


Nutrients ◽  
2017 ◽  
Vol 9 (10) ◽  
pp. 1150 ◽  
Author(s):  
Vinícius Cooper-Capetini ◽  
Diogo de Vasconcelos ◽  
Amanda Martins ◽  
Sandro Hirabara ◽  
José Donato Jr. ◽  
...  

Diabetes ◽  
2011 ◽  
Vol 60 (3) ◽  
pp. 890-898 ◽  
Author(s):  
Michael J. Jurczak ◽  
Hui-Young Lee ◽  
Andreas L. Birkenfeld ◽  
Francois R. Jornayvaz ◽  
David W. Frederick ◽  
...  

2021 ◽  
Vol 60 (9) ◽  
pp. 1433-1442
Author(s):  
Tatsuya Kondo ◽  
Sayaka Kitano ◽  
Nobukazu Miyakawa ◽  
Takuro Watanabe ◽  
Rieko Goto ◽  
...  

2012 ◽  
Vol 49 (1) ◽  
pp. R9-R17 ◽  
Author(s):  
Laura Marroquí ◽  
Alejandro Gonzalez ◽  
Patricia Ñeco ◽  
Ernesto Caballero-Garrido ◽  
Elaine Vieira ◽  
...  

Leptin plays an important role in the control of food intake, energy expenditure, metabolism, and body weight. This hormone also has a key function in the regulation of glucose homeostasis. Although leptin acts through central and peripheral mechanisms to modulate glucose metabolism, the pancreatic β-cell of the endocrine pancreas is a critical target of leptin actions. Leptin receptors are present in the β-cell, and their activation directly inhibits insulin secretion from these endocrine cells. The effects of leptin on insulin occur also in the long term, since this hormone inhibits insulin gene expression as well. Additionally, β-cell mass can be affected by leptin through changes in proliferation, apoptosis, or cell size. All these different functions in the β-cell are triggered by leptin as a result of the large diversity of signaling pathways that this hormone is able to activate in the endocrine pancreas. Therefore, leptin can participate in glucose homeostasis owing to different levels of modulation of the pancreatic β-cell population. Furthermore, it has been proposed that alterations in this level of regulation could contribute to the impairment of β-cell function in obesity states. In the present review, we will discuss all these issues with special emphasis on the effects and pathways of leptin signaling in the pancreatic β-cell.


Author(s):  
S. Neda Mousavy Gharavy ◽  
Bryn Owen ◽  
Steven J. Millership ◽  
Pauline Chabosseau ◽  
Grazia Pizza ◽  
...  

AbstractVariants close to the VPS13C/C2CD4A/C2CD4B locus are associated with altered risk of type 2 diabetes in genome-wide association studies. Whilst previous functional work has suggested roles for VPS13C and C2CD4A in disease development, none has explored the role of C2CD4B. Here, we show that systemic inactivation of C2cd4b in mice leads to marked, but highly sexually dimorphic, changes in body weight and glucose homeostasis. Female C2cd4b mice display unchanged body weight but abnormal glucose tolerance and defective in vivo, but not in vitro, insulin secretion, associated with a marked decrease in follicle stimulating hormone levels. In sharp contrast, male C2cd4b null mice displayed normal glucose tolerance but an increase in body weight and fasting glycemia after maintenance on high fat diet. No metabolic disturbances were observed after global inactivation of C2cd4a in mice, or in pancreatic β cell function at larval stages in C2cd4ab null zebrafish. These studies suggest that C2cd4b may act centrally to influence sex-dependent circuits which control pancreatic β cell function and glucose tolerance in rodents. However, the absence of sexual dimorphism in the impact of diabetes risk variants argues for additional roles for C2CD4A or VPS13C in the control of glucose homeostasis in man.


Diabetes ◽  
2020 ◽  
pp. db200057
Author(s):  
Seokwon Jo ◽  
Amber Lockridge ◽  
Ramkumar Mohan ◽  
Nicholas Esch ◽  
Regina Schlichting ◽  
...  

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