Exogenous glucagon-like peptide-1 reduces body weight and cholecystokinin-8 enhances this reduction in diet-induced obese male rats

Mhalhal, Thaer R.; Washington, Martha C.; Newman, Kayla D.; Heath, John; Sayegh, Ayman I.

doi:10.1016/j.physbeh.2017.06.011

Cited by 9 publications

(4 citation statements)

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“…Therefore, the actions of NS CCK-8, possibly including reduction of food intake, may be peripheral/local i.e., gastrointestinal. Others (Calingasan et al, 1992;Cox et al, 1996;Smith et al, 1988) and we (Mhalhal et al, 2017b;Newman et al, 2017;Sayegh et al, 2015;Washington et al, 2016b) have shown that the gastrointestinal tract is a potential site of action for reduction of food intake by S CCK-8, GRP-29 and GLP-1, (Mhalhal et al, 2017a(Mhalhal et al, , 2018Washington et al, 2014), because intra-arterial infusions of S CCK-8 (0.05 nmol/kg) in the cranial mesenteric artery, which supplies the small intestine, but not ip injections, reduced food intake (Mhalhal et al, 2017a,b;Sayegh et al, 2015;Washington et al, 2016a,b). In addition, interrupting the enteric neurons utilizing a duodenal myotomy procedure also attenuated reduction of food intake by the same peptide (Lateef et al, 2012).…”

Section: Discussionmentioning

confidence: 87%

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

et al. 2019

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Recently, we reported that non-sulfated cholecystokinin-8 (NS CCK-8) reduces food intake by cholecystokinin-B receptors (CCK-BR). To examine a possible site of action for this peptide, and based on the fact that both NS CCK-8 and CCK-BR are found centrally and peripherally, in the current study we hypothesized that NS CCK-8 increases Fos-like immunoreactivity (Fos-LI, a neuronal activation marker) in the dorsal vagal complex (DVC) of the hindbrain and the myenteric and submucosal plexuses of the small intestine. We found that intraperitoneal NS CCK-8 (0.5 nmol/kg) increases Fos-LI in the DVC, the myenteric and the submucosal plexuses of the duodenum and the myenteric plexus of the jejunum. The findings suggest, but does not prove, a potential role for the DVC and the enteric neurons in the feeding responses evoked by NS CCK-8.

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Section: Discussionmentioning

confidence: 87%

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

et al. 2019

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“…Cholecystokinin is the most extensively studied gastrointestinal satiety hormone secreted by the I-cells that line the intestinal tract. The main role of CCK is to promote the secretion of various digestive enzymes from the pancreatic acinus and enhance the release of GLP-1 to reduce food intake (37). In Fig.…”

Section: Resultsmentioning

confidence: 99%

Gastrointestinal and metabolic effects of noodles-based konjac glucomannan in rats

Zhou¹,

Qin²,

Wang³

et al. 2019

Food & Nutrition Research

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This study was conducted to investigate the hypothesis that the beneficial metabolic effects of dietary fiber, konjac glucomannan (KGM), related with in vivo digestion might be altered if the complicated food matrix was taken into consideration. A diet of precooked noodles (PN), as widely produced and consumed in Asia, was used to simulate an actual food context. Assays were conducted with male Wistar rats (n = 80); the rats were divided into five groups and fed with either PN (control), PN supplemented with medium-dose KGM (MK), precooked low-dose KGM-supplemented noodles (LKD), precooked medium-dose KGM-supplemented noodles (MKD) or precooked high-dose KGM supplemented noodles (HKD). The time-dependent changes in blood glucose and the sensitivity to insulin after intragastric administration were determined to evaluate the postprandial glycemic response. The activity of intestinal Na+-K+-ATPase and the levels of gut hormones including motilin, cholecystokin, GLP-1, and orexin were also determined to provide insights into the function of gastrointestinal motion and after-meal hormonal feedback in each group. The noodles-based KGM showed much more efficacy in sustaining glucose homeostasis compared with KGM supplemented in a diet of noodles, indicating there might be potential long-term health outcomes of satiety and energy balance using noodles-based KGM. The postprandial glycemia was largely moderated by LKD and MKD. Despite the significant reduction in the production of glucose, MKD caused insensitivity to insulin–blood glucose regulation and a rapid gut negative feedback following a severe blood glucose fluctuation. In conclusion, the health-promoting benefits of KGM supplements on glycemic response highly depend on the type of matrix and the dose of KGM.

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“…In conclusion, our data indicates interesting associations between the CCKAR rs6448456 polymorphism and the metabolic characteristics of patients with PCOS. Better understanding of the role of genetic variability in CCKAR and CCKBR may be of clinical importance for future development of treatment strategies with CCK receptor agonists, which have already been shown to enhance the weight lowering, appetite suppressing, and positive beta-cell actions of GLP-1 based drugs in preclinical models [27][28][29]. It needs to be pointed out, that the investigated receptor polymorphisms could also play an important role in response to treatment with potential CCK receptor agonists as previously shown for other receptor polymorphisms, for example in liraglutide treatment in obese women with PCOS [30] as well as in other therapeutic fields [31].…”

Section: Discussionmentioning

confidence: 99%

Genetic variability in the cholecystokinin A receptor affects lipid profile and glucose tolerance in patients with polycystic ovary syndrome

et al. 2022

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IntroductionCholecystokinin (CCK) is involved in several metabolic pathways and CCK agonist are considered as potential novel treatment option in populations with increased metabolic risk, including polycystic ovary syndrome (PCOS). As genetic variability of cholecystokinin A and B receptor genes (CCKAR and CCKBR, respectively) may modify its biological actions, we investigated the impact of CCKAR and CCKBR genetic variability on anthropometric and metabolic parameters in patients with PCOS.Material and methodsOur cross-sectional study included 168 patients with PCOS and 82 healthy female controls genotyped for polymorphisms in CCKAR (rs6448456 and rs1800857) and CCKBR (rs2929180, rs1800843, rs1042047 and rs1042048) genes.ResultsThe investigated polymorphisms were not associated with anthropometric characteristics of patients with PCOS, however, among healthy controls carriers of at least one polymorphic CCKBR rs1800843 allele had bigger waist circumference (p=0.027) and more visceral fat (p=0.046). Among PCOS patients carriers of at least one polymorphic CCKAR rs6448456 C allele had significantly higher total blood cholesterol and LDL, and significantly lower blood glucose levels after 30, 60 and 90 minutes of the oral glucose tolerance test (all p<0.05). Healthy controls with at least one polymorphic CCKAR rs1800857 C allele were less likely to have high metabolic syndrome burden (p=0.029).ConclusionsGenetic variability in CCKAR affects lipid profile and post-load glucose levels in patients with PCOS and is associated with metabolic sydrome burden in healthy young women. Further investigation of the role of genetic variability in CCKAR and CCKBR could contribute to development of individually tailored treatment strategies with CCK receptor agonists.

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Exogenous glucagon-like peptide-1 reduces body weight and cholecystokinin-8 enhances this reduction in diet-induced obese male rats

Cited by 9 publications

References 35 publications

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

Gastrointestinal and metabolic effects of noodles-based konjac glucomannan in rats

Genetic variability in the cholecystokinin A receptor affects lipid profile and glucose tolerance in patients with polycystic ovary syndrome

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