Lipid derivatives activate GPR119 and trigger GLP-1 secretion in primary murine L-cells

Moss, Catherine E.; Glass, Leslie; Diakogiannaki, Eleftheria; Pais, Ramona; Lenaghan, Carol; Smith, David M.; Wedin, Marianne; Bohlooly‐Y, Mohammad; Gribble, Fiona M.; Reimann, Frank

doi:10.1016/j.peptides.2015.06.012

Cited by 81 publications

(48 citation statements)

References 27 publications

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“…Similar findings were made in studies involving oleoyldopamide in wt and GPR119‐KO mice . Furthermore, the importance of dietary fat as a trigger of GLP‐1 release through GPR119 was recently demonstrated by the use of wt and GPR119‐KO mice . GPR119‐KO mice appear to have normal islet morphology, body weight and fed/fasted glucose levels .…”

Section: Discussionsupporting

confidence: 77%

Oral 2‐oleyl glyceryl ether improves glucose tolerance in mice through the GPR119 receptor

et al. 2016

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The intestinal G protein-coupled receptor GPR119 is a novel metabolic target involving glucagon-like peptide-1 (GLP-1)-derived insulin-regulated glucose homeostasis. Endogenous and diet-derived lipids, including N-acylethanolamines and 2-monoacylglycerols (2-MAG) activate GPR119. The purpose of this work is to evaluate whether 2-oleoyl glycerol (2-OG) improves glucose tolerance through GPR119, using wild type (WT) and GPR 119 knock out (KO) mice. We here show that GPR119 is essential for 2-OG-mediated release of GLP-1 and CCK from GLUTag cells, since a GPR119 specific antagonist completely abolished the hormone release. Similarly, in isolated primary colonic crypt cultures from WT mice, GPR119 was required for 2-OG-stimulated GLP-1 release while there was no response in crypts from KO mice. In vivo, gavage with 2-oleyl glyceryl ether ((2-OG ether), a stable 2-OG analog with a potency of 5.3 µM for GPR119 with respect to cAMP formation as compared to 2.3 µM for 2-OG), significantly (P < 0.05) improved glucose clearance in WT littermates, but not in GPR119 KO mice. Finally, deletion of GPR119 in mice resulted in lower glucagon levels, whereas the levels of insulin and GIP were unchanged. In the present study we show that 2-OG stimulates GLP-1 secretion through GPR119 activation in vitro, and that fat-derived 2-MAGs are potent candidates for mediating fat-induced GLP-1 release through GPR119 in vivo. © 2016 BioFactors, 42(6):665-673, 2016.

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Section: Discussionsupporting

confidence: 77%

Oral 2‐oleyl glyceryl ether improves glucose tolerance in mice through the GPR119 receptor

et al. 2016

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“…OEA and PEA do not act at cannabinoid receptors, but instead activate peroxisome proliferator-activated receptors (PPARs) that regulate lipid metabolism. OEA attenuates body mass gains and stimulates breakdown of fat through PPAR-á (Fu et al, 2003), but its peripherally-based anorectic effects (Rodriguez de Fonseca et al, 2001) may be in part due to its ability to activate GPR119 and elicit glucagon-like peptide-1 (GLP-1) secretion (Lauffer et al, 2009; Moss et al, 2016), which itself has anorectic effects in the hindbrain (Hayes et al, 2008). Thus we predicted that OEA would function in a direction opposite to that of endocannabinoids with respect to fat regulation; instead, we found that OEA concentrations correlated negatively with adiposity, much like our 2-AG findings.…”

Section: Discussionmentioning

confidence: 99%

Lipid signaling and fat storage in the dark-eyed junco

Burns

Rendon

et al. 2017

General and Comparative Endocrinology

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Seasonal hyperphagia and fattening promote survivorship in migratory and wintering birds, but reduced adiposity may be more advantageous during the breeding season. Factors such as photoperiod, temperature, and food predictability are known environmental determinants of fat storage, but the underlying neuroendocrine mechanisms are less clear. Endocannabinoids and other lipid signaling molecules regulate multiple aspects of energy balance including appetite and lipid metabolism. However, these functions have been established primarily in mammals; thus the role of lipid signals in avian fat storage remains largely undefined. Here we examined relationships between endocannabinoid signaling and individual variation in fat storage in captive white-winged juncos (Junco hyemalis aikeni) following a transition to long-day photoperiods. We report that levels of the endocannabinoid 2-arachidonoylglycerol (2-AG), but not anandamide (AEA), in furcular and abdominal fat depots correlate negatively with fat mass. Hindbrain mRNA expression of CB1 endocannabinoid receptors also correlates negatively with levels of fat, demonstrating that fatter animals experience less central and peripheral endocannabinoid signaling when in breeding condition. Concentrations of the anorexigenic lipid, oleoylethanolamide (OEA), also inversely relate to adiposity. These findings demonstrate unique and significant relationships between adiposity and lipid signaling molecules in the brain and periphery, thereby suggesting a potential role for lipid signals in mediating adaptive levels of fat storage.

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“…An example of regional distinction is that GLP‐1‐secreting cells in the distal jejunum and ileum co‐express PYY, whereas proximal GLP‐1‐secreting cells co‐express CCK, GIP, neurotensin, or secretin . Although, traditionally, these enteroendocrine cells were differentiated by the peptides they secrete, recent research suggests that there is heterogeneous co‐expression of different peptides in these cells, and that these patterns of co‐expression differ between regions of the gGI tract . This process may enable enteroendocrine cells to respond to specific local nutritional stimuli .…”

Section: Mechanisms For Metabolic Successmentioning

confidence: 99%

“…25 Although, traditionally, these enteroendocrine cells were differentiated by the peptides they secrete, recent research suggests that there is heterogeneous co-expression of different peptides in these cells, and that these patterns of co-expression differ between regions of the gGI tract. 26 This process may enable enteroendocrine cells to respond to specific local nutritional stimuli. 27 Bariatric surgeries change not only the GI anatomy, but also the rate at which nutrients enter the intestine.…”

Section: Rygb Vsgmentioning

confidence: 99%

Mechanisms for the metabolic success of bariatric surgery

Sandoval

2019

J Neuroendocrinology

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To date, bariatric surgery remains the most effective strategy for the treatment of obesity and its comorbidities. However, given the enormity of the obesity epidemic, and sometimes variable results, it is not a feasible strategy for the treatment of all obese patients. A simple PubMed search for ‘bariatric surgery' reveals over 28 000 papers that have been published since the 1940s when the first bariatric surgeries were performed. However, there is still an incomplete understanding of the mechanisms for the weight loss and metabolic success of surgery. An understanding of the mechanisms is important because it may lead to greater understanding of the pathophysiology of obesity and thus surgery‐alternative strategies for the treatment of all obese patients. In this review, the potential mechanisms that underlie the success of surgery are discussed, with a focus on the potential endocrine, neural and other circulatory factors (eg, bile acids) that have been proposed to play a role.

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Lipid derivatives activate GPR119 and trigger GLP-1 secretion in primary murine L-cells

Cited by 81 publications

References 27 publications

Oral 2‐oleyl glyceryl ether improves glucose tolerance in mice through the GPR119 receptor

Oral 2‐oleyl glyceryl ether improves glucose tolerance in mice through the GPR119 receptor

Lipid signaling and fat storage in the dark-eyed junco

Mechanisms for the metabolic success of bariatric surgery

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