Intestinal CART is a regulator of GIP and GLP-1 secretion and expression

Shcherbina, Liliya; Lindqvist, Andreas; Fischer, A.-H. Thorén; Ahlqvist, Emma; Zhang, Enming; Falkmer, Sture; Renström, Erik; Koffert, Jukka; Honka, Henri; Wierup, Nils

doi:10.1016/j.mce.2018.04.002

Cited by 11 publications

(11 citation statements)

References 53 publications

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“…GPR68 is an orphan GPCR uniquely expressed by ECs (Figure S6C). The orphan peptide CART (cocaine-and amphetamine-regulated protein) activates GPR68 (Foster et al, 2019); it has a role in the regulation of anxiety, reward, and feeding behaviors (Shcherbina et al, 2018). We find broad expression of the subunit of the GABA-B receptor GABBR2, potentially allowing a GABA response (Figure S7C) (Hyland and Cryan, 2010).…”

Section: High-definition Transcriptomic and Proteomic Profiling Of Eecsmentioning

confidence: 85%

High-Resolution mRNA and Secretome Atlas of Human Enteroendocrine Cells

Beumer

Puschhof

Bauzá‐Martinez

et al. 2020

Cell

146

133

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Section: High-definition Transcriptomic and Proteomic Profiling Of Eecsmentioning

confidence: 85%

High-Resolution mRNA and Secretome Atlas of Human Enteroendocrine Cells

Beumer

Puschhof

Bauzá‐Martinez

et al. 2020

Cell

146

133

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“…Duodenectomy disrupts the relationship between cycles of both interdigestive GI hormone release, and insulin secretion, because of interruption of duodeno-pancreatic neural connections and loss of vagus-sensitive humoral factors. 47,48 sPD and PPPD are associated with an increase of fasting and stimulated GLP-1 levels, which is not translated into higher insulin secretion after PD. GLP-1 stimulates insulin secretion and acts as a neuropeptide to control glucose homeostasis.…”

Section: Discussionmentioning

confidence: 95%

Resection of the duodenum causes long-term endocrine and exocrine dysfunction after Whipple procedure for benign tumors - Results of a systematic review and meta-analysis

Beger

Mayer

Poch

2020

HPB

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Background: Metabolic dysfunctions after pancreatoduodenectomy (PD) need to be considered when pancreatic head resection is likely to lead to long-term survival.Methods: Medline, Embase and Cochrane Library were searched for studies reporting measured data of metabolic function after PD and duodenum-sparing total pancreatic head resection (DPPHR). Data from 23 cohort studies comprising 1019 patients were eligible; 594 and 910 patients were involved in systematic review and meta-analysis, respectively. Results:The cumulative incidence of postoperative new onset of diabetes mellitus (pNODM) after PD for benign tumors was 46 of 321 patients (14%) measured after follow-up of in mean 36 months postoperatively. New onset of postoperative exocrine insufficiency (PEI) was exhibited by 91 of 209 patients (44%) after PD for benign tumors measured in mean 23 months postoperatively. The meta-analysis indicated pNODM after PD for benign tumor in 32 of 208 patients (15%) and in 10 of 178 patients (6%) after DPPHR (p = 0.007; OR 3.01; (95%CI:1.39-6.49)). PEI was exhibited by 80 of 178 patients (45%) after PD and by 6 of 88 patients (7%) after DPPHR (p < 0.001). GI hormones measured in 194 patients revealed postoperatively a significant impairment of integrated responses of gastrin, motilin, insulin, secretin, PP and GIP (p < 0.050-0.001) after PD. Fasting and stimulated levels of GLP-1 and glucagon levels displayed a significant increase (p < 0.020/p < 0.030). Following DPPHR, responses of gastrin, motilin, secretin and CCK displayed no change compared to preoperative levels. Conclusions: After PD, duodenectomy, rather than pancreatic head resection is the main cause for long-term persisting, postoperative new onset of DM and PEI.

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“…Curiously, the feeling of satiety, is also achieved by another neurotransmitter, the Cocaine- and amphetamine-regulated transcript (CART) ( 161 ). This peptide, acts also as a hormone, and is expressed by both β-cells and intestinal GLP-1 and GIP producing cells causing GLP-1 secretion in vivo via a yet unknown GPCR ( 162 ).…”

Section: The Physiology Of Glp-1mentioning

confidence: 99%

Dissecting the Physiology and Pathophysiology of Glucagon-Like Peptide-1

Paternoster

Falasca

2018

Front. Endocrinol.

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An aging world population exposed to a sedentary life style is currently plagued by chronic metabolic diseases, such as type-2 diabetes, that are spreading worldwide at an unprecedented rate. One of the most promising pharmacological approaches for the management of type 2 diabetes takes advantage of the peptide hormone glucagon-like peptide-1 (GLP-1) under the form of protease resistant mimetics, and DPP-IV inhibitors. Despite the improved quality of life, long-term treatments with these new classes of drugs are riddled with serious and life-threatening side-effects, with no overall cure of the disease. New evidence is shedding more light over the complex physiology of GLP-1 in health and metabolic diseases. Herein, we discuss the most recent advancements in the biology of gut receptors known to induce the secretion of GLP-1, to bridge the multiple gaps into our understanding of its physiology and pathology.

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Intestinal CART is a regulator of GIP and GLP-1 secretion and expression

Cited by 11 publications

References 53 publications

High-Resolution mRNA and Secretome Atlas of Human Enteroendocrine Cells

High-Resolution mRNA and Secretome Atlas of Human Enteroendocrine Cells

Resection of the duodenum causes long-term endocrine and exocrine dysfunction after Whipple procedure for benign tumors - Results of a systematic review and meta-analysis

Dissecting the Physiology and Pathophysiology of Glucagon-Like Peptide-1

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