Faculty Opinions recommendation of Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes.

Author(s):  
Michael Schwartz ◽  
Jarrad Scarlett
2012 ◽  
Vol 18 (6) ◽  
pp. 950-955 ◽  
Author(s):  
Danna M Breen ◽  
Brittany A Rasmussen ◽  
Andrea Kokorovic ◽  
Rennian Wang ◽  
Grace W C Cheung ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1806-P ◽  
Author(s):  
QINGTAO YAN ◽  
NA LI ◽  
RUIYAN PAN ◽  
HUAI-JIE WANG ◽  
BIN JIANG ◽  
...  

Epigenomics ◽  
2021 ◽  
Author(s):  
Ghazal Aghagoli ◽  
Andrew Del Re ◽  
Naohiro Yano ◽  
Zhiqi Zhang ◽  
Ahmad Aboul Gheit ◽  
...  

Background: Epigenomic changes occurring during surgery have been neglected in research; diabetes and hypertension can affect the epigenome but little is known about the epigenetics of skeletal muscle (SKM). Methods: DNA methylation was profiled via Illumina MethylationEPIC arrays in SKM samples obtained at the beginning and end of heart surgery with cardiopulmonary bypass. Results: Methylation in patients with hypertension and diabetes was significantly different, more so for uncontrolled diabetes; hypertension alone produced minimal effect. The affected pathways involved IL-1, IL-12, IL-18, TNF-α, IFNγ, VEGF, NF-κB and Wnt signaling, apoptosis and DNA damage response. Significant changes occurred during surgery and included loci in the Hippo–YAP/TAZ pathway. Conclusion: Cardiopulmonary bypass surgery affects the SKM methylome, and the combination of hypertension and diabetes induces changes in the SKM epigenome in contrast to hypertension alone.


2015 ◽  
Vol 26 (2) ◽  
pp. 261-268 ◽  
Author(s):  
Jie Chai ◽  
Guangyong Zhang ◽  
Shaozhuang Liu ◽  
Chunxiao Hu ◽  
Haifeng Han ◽  
...  

2012 ◽  
Vol 8 (4) ◽  
pp. 375-380 ◽  
Author(s):  
Ricardo Cohen ◽  
Pedro Paulo Caravatto ◽  
Jose Luis Correa ◽  
Patricia Noujaim ◽  
Tarissa Zanata Petry ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Aruchuna Ruban ◽  
Hutan Ashrafian ◽  
Julian P. Teare

The rapid rise of obesity and type 2 diabetes poses a global threat to healthcare and is a major cause of mortality and morbidity. Bariatric surgery has revolutionised the treatment of both these conditions but is invasive and associated with an increased risk of complications. The EndoBarrier is a device placed endoscopically in the duodenum, which is designed to mimic the effects of gastric bypass surgery with the aim of inducing weight loss and improving glycaemic control. This review outlines the current clinical evidence of the device, its efficacy, potential mechanisms of action, and utility in clinical practice.


2013 ◽  
Vol 304 (7) ◽  
pp. G635-G645 ◽  
Author(s):  
Bing Li ◽  
Yarong Lu ◽  
Coimbatore B. Srikant ◽  
Zu-Hua Gao ◽  
Jun-Li Liu

The antidiabetic mechanism of bariatric surgery includes specific changes in the secretion of incretins. To identify additional players originating from the gut, we evaluated the effects of duodenal-jejunal bypass (DJB) in morbidly obese Zucker fatty rats. A fast relief of hyperglycemia and hyperinsulinemia was achieved even before a significant weight loss occurred. Fourteen days after DJB, we characterized the changes in intestinal histochemistry in the bypassed duodenum and shortcut jejunum that was reanastomosed directly to the starting point of the duodenum and compared with the corresponding regions of sham-operated rats. The bypassed duodenum exhibited mucosal atrophy and apoptosis and decreased proliferative renewal. In shortcut jejunum, DJB resulted in 40% significantly enlarged intestinal circumference and increased epithelial proliferation, especially in putative transit-amplifying (TA) cells and the crypt. Because Reg family proteins promote cell growth and survival, we explored their expression in the intestine. With the use of immunohistochemistry, Reg1, -3α, and -3β were normally expressed in intestinal mucosa. After DJB, the level of Reg1 protein was reduced, whereas Reg3α and -3β were not changed in bypassed duodenum. Downstream in shortcut jejunum, the levels of Reg1 and -3β were greatly induced and especially concentrated in the putative TA cells. Our results revealed significant changes in the integrity and proliferation of the intestinal mucosa as a consequence of DJB, and in cell- and isoform-specific expression of Reg proteins within the replicating mucosal epithelium, and provide evidence indicating that the activation of Reg proteins may contribute to intestinal compensation against increased load and/or to improving insulin sensitivity.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2023-P
Author(s):  
JINGJING NIU ◽  
JONATHAN D. DOUROS ◽  
JONATHAN CAMPBELL ◽  
MEGAN CAPOZZI ◽  
SARAH M. GRAY ◽  
...  

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1529 ◽  
Author(s):  
Madusha Peiris ◽  
Rubina Aktar ◽  
Sarah Raynel ◽  
Zheng Hao ◽  
Michael Mumphrey ◽  
...  

Background: Nutrient-sensing receptors located on enteroendocrine (EEC) cells modulate appetite via detection of luminal contents. Colonic ‘tasting’ of luminal contents may influence changes to appetite observed in obesity and after weight loss induced by bariatric surgery. We assessed the effects of obesity and gastric bypass-induced weight loss on expression of nutrient-sensing G-protein coupled receptors (GPCRs), EEC and enterochromaffin (EC) cells and mucosal innervation. Methods: qPCR and immunohistochemistry were used to study colonic tissue from (a) chow-fed/lean, (b) high-fat fed/obese, (c) Roux-en-Y gastric bypass surgery (RYGB), and (d) calorie restriction-induced weight loss mice. Results: Expression of GPR41, GPR43, GPR40, GPR120, GPR84, GPR119, GPR93 and T1R3 was increased in obese mice. Obesity-induced overexpression of GPR41, 40, 84, and 119 further increased after RYGB whereas GPR120 and T1R3 decreased. RYGB increased TGR5 expression. L-cells, but not EC cells, were increased after RYGB. No differences in mucosal innervation by protein gene product (PGP) 9.5 and GLP-1R-positive nerve fibers were observed. Stimulation of colonic mucosa with GPR41, GPR40, GPR85, GPR119, and TGR5 agonists increased cell activation marker expression. Conclusions: Several nutrient-sensing receptors induced activation of colonic EEC. Profound adaptive changes to the expression of these receptors occur in response to diet and weight loss induced by RYGB or calorie restriction.


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