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        Sweet Taste-Sensing Receptors Expressed in Pancreatic ß-Cells: Sweet Molecules Act as Biased Agonists

        Itaru Kojima,Yuko Nakagawa,Yoshiaki Ohtsu,Anya Medina,Masahiro Nagasawa 대한내분비학회 2014 Endocrinology and metabolism Vol.29 No.1

        The sweet taste receptors present in the taste buds are heterodimers comprised of T1R2 and T1R3. This receptor is also expressed in pancreatic ß-cells. When the expression of receptor subunits is determined in ß-cells by quantitative reverse transcription polymerase chain reaction, the mRNA expression level of T1R2 is extremely low compared to that of T1R3. In fact, the expression of T1R2 is undetectable at the protein level. Furthermore, knockdown of T1R2 does not affect the effect of sweet molecules, whereas knockdown of T1R3 markedly attenuates the effect of sweet molecules. Consequently, a homodimer of T1R3 functions as a receptor sensing sweet molecules in ß-cells, which we designate as sweet taste-sensing receptors (STSRs). Various sweet molecules activate STSR in ß-cells and augment insulin secretion. With regard to intracellular signals, sweet molecules act on STSRs and increase cytoplasmic Ca2+ and/or cyclic AMP (cAMP). Specifically, when an STSR is stimulated by one of four different sweet molecules (sucralose, acesulfame potassium, sodium saccharin, or glycyrrhizin), distinct signaling pathways are activated. Patterns of changes in cytoplasmic Ca2+ and/or cAMP induced by these sweet molecules are all different from each other. Hence, sweet molecules activate STSRs by acting as biased agonists.

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        Lower SMI is a risk factor for dysphagia in Japanese hospitalized patients with osteoporotic vertebral and hip fracture: A retrospective study

        Kaoru Suseki,Masaomi Yamashita,Yoshiaki Kojima,Yojiro Minegishi,Koichiro Komiya,Masashi Takaso 대한골다공증학회 2022 Osteoporosis and Sarcopenia Vol.8 No.4

        Objectives: Many patients with osteoporotic fragile fracture often suffer from dysphagia that results in malnutrition, further deterioration of physical strength, and rehabilitation difficulties. This study aims to investigate the risk factors for dysphagia in hospitalized patients with osteoporotic vertebral and/or hip fractures. Methods: Between January 2020 and December 2021, 569 inpatients were managed for osteoporotic vertebral or hip fractures. Of these, 503 patients were analyzed and 66 were excluded as the required data could not be obtained or dysphagia with causative diseases such as cerebrovascular disease. The patients were divided into 2 groups: patients with dysphagia (P-group) and patients without dysphagia (N-group). We investigated gender, fracture site, age, systemic skeletal muscle mass index (SMI), bone mineral density (BMD), and body mass index (BMI) in early stage of hospitalization and studied their relationship with dysphagia. Results: There were no significant differences in gender and fracture site between the 2 groups. A significant difference was observed in age, SMI, BMD, and BMI (P < 0.01). We performed a logistic regression analysis with the P-group as the objective variable and age, SMI, BMD, and BMI as explanatory variables. We divided objective groups into all patients, patients with vertebral fracture, patients with hip fracture, men, and women. SMI was an independent risk factor in all groups. Conclusions: Lower SMI was a risk factor for dysphagia in hospitalized patients with osteoporotic vertebral and hip fractures. We carefully observed swallowing function of patients with decreased SMI to maintain the nutritional status and prevent rehabilitation difficulties.

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