scholarly journals Engineered Commensal Bacteria Reprogram Intestinal Cells Into Glucose-Responsive Insulin-Secreting Cells for the Treatment of Diabetes

Diabetes ◽  
2015 ◽  
Vol 64 (5) ◽  
pp. 1794-1803 ◽  
Author(s):  
Franklin F. Duan ◽  
Joy H. Liu ◽  
John C. March
Keyword(s):  
Commensal Bacteria ◽  
Intestinal Cells ◽  
Insulin Secreting Cells ◽  
Treatment Of Diabetes

Gastrointestinal Stem Cells I. Pancreatic stem cells

2005 ◽  
Vol 289 (2) ◽  
pp. G177-G180 ◽  
Author(s):  
Bernat Soria ◽  
Francisco J. Bedoya ◽  
Franz Martin
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Adult Stem Cells ◽  
Cell Types ◽  
Diabetic Animal ◽  
Sufficient Evidence ◽  
Β Cells ◽  
Pancreatic Stem Cells ◽  
Insulin Secreting Cells ◽  
Treatment Of Diabetes

The transplantation of islets isolated from donor pancreas has renewed the interest in cell therapy for the treatment of diabetes. In addition, the capacity that stem cells have to differentiate into a wide variety of cell types makes their use ideal to generate β-cells for transplantation therapies. Several studies have reported the generation of insulin-secreting cells from embryonic and adult stem cells that normalized blood glucose values when transplanted into diabetic animal models. Finally, although much work remains to be done, there is sufficient evidence to warrant continued efforts on stem cell research to cure diabetes.

scholarly journals Fatty acids produced by the gut microbiota dampen host inflammatory responses by modulating intestinal SUMOylation

2022 ◽  
Author(s):  
Chaima Ezzine ◽  
Lea Loison ◽  
Christine Bole-Feysot ◽  
Pierre Dechelotte ◽  
Moise Coeffier ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Gut Microbiota ◽  
Inflammatory Responses ◽  
Commensal Bacteria ◽  
Intestinal Cell ◽  
Intestinal Cells ◽  
Dependent Manner ◽  
Intestinal Physiology ◽  
Nf Kappab ◽  
Chain Fatty Acids

The gut microbiota produces a wide variety of metabolites, which interact with intestinal cells and contribute to host physiology. These metabolites regulate intestinal cell activities by modulating either gene transcription or post-translational modifications of gut proteins. The effect of gut commensal bacteria on SUMOylation, an essential ubiquitin-like modification in intestinal physiology, remains however unknown. Here, we show that short chain fatty acids (SCFAs) and branched chain fatty acids (BCFAs) produced by the gut microbiota increase protein SUMOylation in different intestinal cell lines in a pH-dependent manner. We demonstrate that these metabolites induce an oxidative stress which inactivates intestinal deSUMOylases and promotes the hyperSUMOylation of chromatin-bound proteins. In order to determine the impact of these modifications on intestinal physiology, we focused on the NF-kappaB signaling pathway, a key player in inflammation known to be regulated by SUMOylation. We demonstrated that the hyperSUMOylation induced by SCFAs/BCFAs inhibits the activation of the NF-kappaB pathway in intestinal cells by blocking the degradation of the inhibitory factor IkappaBalpha in response to TNFalpha. This results in a decrease in pro-inflammatory cytokines expression, such as IL8 or CCL20, as well as a decrease in intestinal epithelial permeability in response to TNFalpha. Together, our results reveal that fatty acids produced by gut commensal bacteria regulate intestinal physiology by modulating SUMOylation and illustrate a new mechanism of dampening of host inflammatory responses by the gut microbiota.

Glucokinase activators: molecular tools for studying the physiology of insulin-secreting cells

2007 ◽  
Vol 35 (5) ◽  
pp. 1208-1210 ◽  
Author(s):  
D. Johnson ◽  
R.M. Shepherd ◽  
D. Gill ◽  
T. Gorman ◽  
D.M. Smith ◽  
...  
Keyword(s):  
Human Islets ◽  
Significant Advance ◽  
Cell Physiology ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Rate Limiting Step ◽  
Glucokinase Activators ◽  
Insulin Secreting Cells ◽  
Treatment Of Diabetes

GK (glucokinase) catalyses the phosphorylation of glucose to glucose 6-phosphate in glucosensitive cells. In pancreatic β-cells, this reaction is the rate-limiting step of insulin release. Recent work has led to the discovery of synthetic small-molecule activators of GK that stimulate β-cell physiology and subsequently enhance the glucose-dependent release of insulin. It is currently recognized that these compounds may represent a significant advance in the development of new agents in the treatment of diabetes. In addition, GKAs (GK activators) are emerging as reagents that are useful tools with which to probe the function of pancreatic β-cells and other glucosensitive cells. This includes providing insights into the physiology of the β-cell by helping to elucidate the kinetic cycle of GK, confirming the central role of glucose metabolism to the β-cell and highlighting subtle species-dependent differences in insulin secretion between rodent and human islets of Langerhans.

Treatment of diabetes mellitus: Implications of the use of oral agents

1999 ◽  
Vol 138 (4) ◽  
pp. s334-s337 ◽  
Author(s):  
S RAO ◽  
A BETHEL ◽  
M FEINGLOS
Keyword(s):  
Diabetes Mellitus ◽  
Oral Agents ◽  
Treatment Of Diabetes

Iron-induced expression of BMP6 in intestinal cells is the main regulator of hepatic hepcidin expression in vivo

2010 ◽  
Vol 48 (01) ◽  
Author(s):  
S Arndt ◽  
U Mägdefrau ◽  
C Dorn ◽  
K Schardt ◽  
AK Bosserhoff ◽  
...  
Keyword(s):  
Intestinal Cells ◽  
Induced Expression ◽  
Hepcidin Expression ◽  
Main Regulator

Tapping the Philippines' Rich Biodiversity for the Treatment of Diabetes

Planta Medica ◽  
2013 ◽  
Vol 79 (05) ◽  
Author(s):  
EC Amor ◽  
L Tolosa ◽  
FC Macazo ◽  
MD Naing
Keyword(s):  
The Philippines ◽  
Treatment Of Diabetes

Insulin Initiation and Concomitant OHA (Oral Hypoglycaemic Agents) in Treatment of Diabetes Mellitus—Results of the Indian Human Insulin Registry (INHIRIT)

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2293-PUB ◽  
Author(s):  
VEERANNA KARADI ◽  
DILIP PAWAR ◽  
SARAH JABEEN ◽  
SANDEEP S. ◽  
SAPTARSHI BOSE ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Human Insulin ◽  
Insulin Initiation ◽  
Oral Hypoglycaemic Agents ◽  
Hypoglycaemic Agents ◽  
Treatment Of Diabetes
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