Evidence mapPaperPMID 42420684Full record

ArticleHormones (Athens, Greece)2026

Highly selective SGLT2 inhibitors suppress glucose uptake in alpha-TC1 cells, while glucagon secretion is not affected.

Licht Miyamoto, Suguru Nakayama, Honoka Endoh, Kano Fujiwara, Mana Hattori, Takashi Yasuoka, Masaki Imanishi, Yasumasa Ikeda, Koichiro Tsuchiya

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Article in Hormones (Athens, Greece), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Licht MiyamotoDepartment of Nutrition and Life Science, Laboratory of Physiology, Pharmacology and Food Science, Faculty of Health and Medical Sciences, Kanagawa Institute of Technology, Shimo-Ogino, Atsugi-Shi, Kanagawa, 1030243-0292, Japan. licht_corresp2011@yahoo.co.jp.ORCID http://orcid.org/0000-0003-2331-964X
Suguru NakayamaDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Honoka EndohDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Kano FujiwaraDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Mana HattoriDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Takashi YasuokaDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Masaki ImanishiDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.
Yasumasa IkedaDepartment of Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 3-18-15, Kuramoto-Cho, Tokushima, 770-8505, Japan.
Koichiro TsuchiyaDepartment of Medical Pharmacology, Institute of Biomedical Sciences, Graduate School of Tokushima University, 1-78-1, Sho-Machi, Tokushima, 770-8505, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe existence of sodium-glucose cotransporter 2 (SGLT2) in pancreatic alpha cells and its potential roles in glucagon secretion remain controversial despite its well-established function in renal glucose reabsorption. While some studies suggest SGLT2 presence and its involvement in glucagon regulation, others report no expression in alpha cells.

methodsTo clarify this dispute, we investigated the acute functional effects of the highly selective SGLT2 inhibitors dapagliflozin and empagliflozin on glucose uptake, intracellular ATP levels, and glucagon secretion in alpha-TC1 cells, a widely used model of glucagon-secreting cells in culture.

resultsThe SGLT2 inhibitors significantly suppressed basal glucose uptake in alpha-TC1 cells, suggesting the presence of functional SGLT2. However, the inhibitors did not affect glucagon secretion. Neither the SGLT2 inhibitors nor the more potent glucose transport inhibitor, cytochalasin B, altered intracellular ATP levels or glucagon secretion. In contrast, pharmacological inhibition of K/ATP channels increased glucagon secretion without affecting glucose uptake or ATP levels.

conclusionThese results suggest that while SGLT2 is functionally present at low levels and mediates basal glucose uptake in alpha-TC1 cells, its inhibition has insufficient influence on intracellular ATP levels, and therefore, glucagon secretion remains stable. Furthermore, our observations support predominant involvement of K/ATP channels in regulating glucagon secretion.

Indexed as

Alpha-TC1 cellsGlucagon secretionGlucose uptakePancreatic alpha cellsSGLT2 (sodium-glucose cotransporter 2)

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.