Insulinotropic action of β-<scp>l</scp>-glucose pentaacetate

Malaisse, Willy; Best, Leonard; Herchuelz, André; Hiriart, Marcia; Jijakli, Hassan; Kadiata, Marcel; Larrieta-Carasco, Elena; Laghmich, Aouatif; Louchami, Karim; Mercan, Dany; Olivares, Elizabeth; Sánchez-Soto, Carmen; Scruel, Olivier; Sener, Abdullah; Valverde, Isabel; Villanueva-Peñacarrillo, María Luisa; Viñambres, Concepción; Zawalich, Walter S.

doi:10.1152/ajpendo.1998.275.6.e993

Cited by 5 publications

(2 citation statements)

References 28 publications

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“…[39] high-fat diet-fed mice mouse Supplementation of luteolin in diet promoted thermogenesis in BAT and subcutaneous adipose tissue. [40] primary adipocytes human Silibinin increases thermogenic marker genes [41] Liver high-fat diet-fed mice mouse Supplementation of oleuropein to diet reduced liver weight and hepatic triglyceride level [47] diet-induced obese mice mouse Oral gavage of KDT501 reduced lipid deposition of the liver [48] high-fat diet-fed mice mouse Supplementation of epigallocatechin-3-gallate to diet reduced hepatic lipid and cholesterol content [49] Islet HIT-T15 cells isolated islet hamster rat Denatonium benzoate induces insulin secretion [50] isolated islet rat β-L-Glucose pentaacetate induces insulin secretion [51]…”

Section: Nci-h716cellsmentioning

confidence: 99%

“…The GTEx database also shows that TAS2R3, 4, 5, 10, 14, 19, 20, and 31 are expressed in the pancreas (Figure 1); however, the role of T2Rs in the pancreas has not been carefully studied. Nonetheless, some bitter compounds have been reported to induce insulin secretion in isolated pancreatic islets, including denatonium benzoate and β-L-glucose pentaacetate [50,51]. One study showed that the effect of denatonium benzoate on insulin secretion was apparently mediated by a transducin-independent pathway, involving a decrease in ATP-sensitive potassium (KATP) channel activity, depolarization of β-cells, and increased Ca 2+ influx [50], casting doubt on the involvement of T2Rs.…”

Section: Pancreatic Isletsmentioning

confidence: 99%

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Association of Bitter Taste Receptors with Obesity and Diabetes and Their Role in Related Tissues

Kato,

Oshima

2023

Receptors

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Taste 2 receptors (T2Rs) are G-protein-coupled receptors responsible for sensing bitter tastes. Many studies have shown the expression of T2Rs in extraoral tissues and the unique role of T2Rs in each tissue. Single-nucleotide polymorphisms of T2Rs are associated with the risk of obesity and diabetes, and the organs/tissues associated with the development of these metabolic diseases, including the intestine, adipose, muscle, liver, and pancreas, are reported to express T2R genes. This result suggests that T2Rs in extraoral tissues contribute to the development of obesity and diabetes. In this narrative review, we summarize current knowledge of the associations of T2Rs with obesity and diabetes, provide an overview of extraoral tissues that are associated with the development of obesity and diabetes that express T2R genes, and summarize the current knowledge of T2Rs.

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Section: Nci-h716cellsmentioning

confidence: 99%

Section: Pancreatic Isletsmentioning

confidence: 99%

Association of Bitter Taste Receptors with Obesity and Diabetes and Their Role in Related Tissues

Kato,

Oshima

2023

Receptors

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Insulin release: the receptor hypothesis

Malaisse

2014

Diabetologia

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It is currently believed that the stimulation of insulin release by nutrient secretagogues reflects their capacity to act as fuel in pancreatic islet beta cells. In this review, it is proposed that such a fuel concept is not incompatible with a receptor hypothesis postulating the participation of cell-surface receptors in the recognition of selected nutrients as insulinotropic agents. Pursuant to this, attention is drawn to such matters as the anomeric specificity of the beta cell secretory response to D-glucose and its perturbation in diabetes mellitus, the insulinotropic action of artificial sweeteners, the possible role of bitter taste receptors in the stimulation of insulin secretion by L-glucose pentaacetate, the recently documented presence of cell-surface sweet taste receptors in insulin-producing cells, the multimodal signalling process resulting from the activation of these latter receptors, and the presence in beta cells of a sweet taste receptor mediating the fructose-induced potentiation of glucose-stimulated insulin secretion.

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Insulinotropic action of monosaccharide esters: therapeutic perspectives

Malaisse¹

1999

Diabetologia

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Keywords Monosaccharide esters, insulin release.Several monosaccharide esters were recently introduced as new tools in biomedical research. [1]. These esters seem to be able to cross the plasma membrane without requiring the intervention of a specific carrier system. They then undergo intracellular hydrolysis in esterase-catalysed reactions, so that their glucidic moiety becomes readily available for further metabolism or metabolic action [2,3]. The major aim of this brief review is to draw attention to the possible use of some of these esters as new insulinotropic tools in the treatment of such diseases as Type II (non-insulin-dependent) diabetes mellitus, insulinoma or persistent hyperinsulinaemia in childhood. In the treatment of diabetes, they could be used in combination with other insulinotropic agents such as hypoglycaemic sulphonylureas Experimental findingsEsters of metabolized hexoses, such as a-d-glucose pentaacetate or b-d-glucose pentaacetate, stimulate insulin release from islets incubated either in the absence of any exogenous nutrient or in the presence of such nutrient secretagogues as d-glucose and l-leucine [47] or, as shown in Figure 1, the dimethyl ester of succinic acid (SAD). Unexpectedly, however, some esters of non-metabolized hexoses, such as a-l-glucose pentaacetate and b-l-glucose pentaacetate also show positive insulinotropic action, the most obvious effect being in islets exposed to another nutrient secretagogue, e. g. l-leucine or the dimethyl ester of succinic acid (Fig. 1). Even more surprisingly, monosaccharide esters that inhibit d-glucose metabolism (such as d-mannoheptulose hexaacetate or 2-deoxy-d-glucose tetraacetate) and suppress d-glucose-stimulated insulin release [48, 49], were found to enhance the beta cell secretory response to non-glucidic nutrients, e. g. the dimethyl ester of succinic acid (Fig. 1). When tested in suitably low concentrations, the tetraacetate esters of 2-deoxy-d-glucose even enhance insulin release stimulated by d-glucose [49].Detailed investigations on the metabolic fate of bl-glucose pentaacetate in isolated pancreatic islets and its effects on variables such as protein biosynthesis, cyclic AMP formation, generation of inositol phosphates, intracellular pH, 86 Rb efflux and bioelectrical activity, 45 Ca net uptake and efflux, cytosolic Ca 2+ concentration and insulin release suggest that the esters of non-metabolized monosaccharides with positive insulinotropic action may directly interact with a receptor system, resulting in a decrease in K + conductance, plasma membrane depolarization and induction of electrical activity [50]. This model is thought to have analogies with the recognition of bitter compounds by taste buds [51]. Purified islet beta cells indeed contain the a-gustducin G-protein involved in this recognition process (unpublished observation).The findings mentioned above also raise the idea that some monosaccharide esters, especially those of l-glucose, can be used as insulinotropic tools to stimulate insulin release in Type ...

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Insulinotropic action of β-l-glucose pentaacetate

Cited by 5 publications

References 28 publications

Association of Bitter Taste Receptors with Obesity and Diabetes and Their Role in Related Tissues

Association of Bitter Taste Receptors with Obesity and Diabetes and Their Role in Related Tissues

Insulin release: the receptor hypothesis

Insulinotropic action of monosaccharide esters: therapeutic perspectives

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