Low extracellular magnesium does not impair glucose-stimulated insulin secretion

Gommers, Lisanne M. M.; Hill, Thomas J.; Ashcroft, Frances M.; Baaij, Jeroen H. F. de

doi:10.1371/journal.pone.0217925

Cited by 19 publications

(19 citation statements)

References 24 publications

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“…3B and S3). TRPM7 channel control of β-cell insulin secretion is also exemplified by a recent report showing that TRPM7 channel knockdown in rat insulinoma cells (INS-1) augments insulin secretion [41]. Taken together, these data suggest that TRPM7 channels not only play an important role in -cell development, but also in limiting insulin secretion.…”

Section: Trpm7 Channels Control -Cell Insulin Secretionsupporting

confidence: 52%

TRPM7 is a critical regulator of pancreatic endocrine development and high-fat diet-induced β-cell proliferation

Altman

Schaub

Dickerson

et al. 2020

Preprint

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The melastatin subfamily of the transient receptor potential channels (TRPM) are regulators of pancreatic β-cell function. TRPM7 is the most abundant islet TRPM channel; however, the role of TRPM7 in β-cell function has not been determined. Here, we utilized various spatiotemporal transgenic mouse models to investigate how TRPM7 knockout influences pancreatic endocrine development, proliferation, and function. Ablation of TRPM7 within pancreatic progenitors reduced pancreatic size, as well as α-cell and β-cell mass. This resulted in impaired glucose tolerance due to decreased serum insulin levels. However, ablation of TRPM7 following endocrine specification or in adult mice did not impact endocrine expansion or glucose tolerance. As TRPM7 regulates cell proliferation, we assessed how TRPM7 influences β-cell hyperplasia under insulin resistant conditions. β-cell proliferation induced by high-fat diet was significantly decreased in TRPM7 deficient β-cells. The endocrine roles of TRPM7 may be influenced by cation flux through the channel, and indeed we find that TRPM7 ablation alters β-cell intracellular Mg2+. Together, these findings reveal that TRPM7 controls pancreatic progenitor expansion and β-cell proliferation, which is likely due to regulation of Mg2+ homeostasis.SummaryThis manuscript identifies a critical developmental role for TRPM7 channels in pancreatic progenitor cells. The manuscript also determines that TRPM7 plays a key role in β-cell proliferation under insulin-resistant conditions.

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Section: Trpm7 Channels Control -Cell Insulin Secretionsupporting

confidence: 52%

TRPM7 is a critical regulator of pancreatic endocrine development and high-fat diet-induced β-cell proliferation

Altman

Schaub

Dickerson

et al. 2020

Preprint

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“…This is not surprising given that expression of TRPM7 is almost ubiquitous. In mouse islets, expression of TRPM7 is eight times higher than that of TRPM6, which is the other Mg 2+ channel present in the mouse islets [110]. In human β-cells TRPM6 is not expressed.…”

Section: Trpm6 and Trpm7mentioning

confidence: 89%

“…Deficiency of TRPM7 reduces total cellular Mg 2+ at least in some cells [111]. Knockdown of Trpm7 in INS-1 cells by siRNA increases insulin secretion in response to glucose [110]. It appears that TRPM7 plays a role in mediating glucose-induced insulin secretion possibly by regulating the cytoplasmic Mg 2+ concentration.…”

Section: Trpm6 and Trpm7mentioning

confidence: 99%

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Molecular Regulations and Functions of the Transient Receptor Potential Channels of the Islets of Langerhans and Insulinoma Cells

Islam

2020

Cells

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Insulin secretion from the β-cells of the islets of Langerhans is triggered mainly by nutrients such as glucose, and incretin hormones such as glucagon-like peptide-1 (GLP-1). The mechanisms of the stimulus-secretion coupling involve the participation of the key enzymes that metabolize the nutrients, and numerous ion channels that mediate the electrical activity. Several members of the transient receptor potential (TRP) channels participate in the processes that mediate the electrical activities and Ca2+ oscillations in these cells. Human β-cells express TRPC1, TRPM2, TRPM3, TRPM4, TRPM7, TRPP1, TRPML1, and TRPML3 channels. Some of these channels have been reported to mediate background depolarizing currents, store-operated Ca2+ entry (SOCE), electrical activity, Ca2+ oscillations, gene transcription, cell-death, and insulin secretion in response to stimulation by glucose and GLP1. Different channels of the TRP family are regulated by one or more of the following mechanisms: activation of G protein-coupled receptors, the filling state of the endoplasmic reticulum Ca2+ store, heat, oxidative stress, or some second messengers. This review briefly compiles our current knowledge about the molecular mechanisms of regulations, and functions of the TRP channels in the β-cells, the α-cells, and some insulinoma cell lines.

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“…Literatürde DM patogenezinde, düşük Mg düzeyinin insülin salınımında bozulma, insülin direnci gelişimi ve kötü glisemik kontrol ile ilişkili olabileceğini öne süren yayınlar mevcuttur (5). Diğer yandan son yıllarda yapılan bazı çalışmalarda hücre dışı Mg düzeyinin insülin sekresyonu üzerine belirgin bir etkisinin olmadığı gösterilmiştir (6). Bu çalışmada, DM hastalarında Mg düzeyi ile glukoz regülasyonu, proteinüri ve metabolik parametreler arasındaki ilişkilerin incelenmesi amaçlandı.…”

Section: Introductionunclassified

The Relationship between Magnesium Level with Glucose Regulation and Amount of Proteinuria in Type 2 Diabetes

Kırık¹,

Ata²,

Bozyel³

2019

JSTR

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Diabetes Mellitus is a globally common, chronic metabolic disease. In progression of disease itself, peripheral insülin resistance and insülin secretion disorders can be observed. In addition there can be electrolyte disorders such as magnesium, calcium and iron deficiency. Magnesium levels may have significant role in the clinical course of the disease. In this study, it is aimed to observe relationship among magnesium levels glucose regulation and proteinuria. In this cross sectional study, 200 diabetic patients were examined for magnesium levels. Blood parameters and proteinuria levels were determined and the patients were divided into two groups as hypomagnesemic and normomagnesemic. Glucose levels, HbA1c and proteinuria levels were compared between groups. Of the cases (n=200), 59 (29.5 %) were male and 141 (70.5 %) were female. The frequency of hypomagnesemia was 38.5 %. The incidence of hypomagnesemia in women (46.1 %) was significantly higher than in men (20.3 %) (p=0.001). In hypomagnesemia group, glucose level (179.7 ± 60.2 mg/dL) was higher than normomagnesemia group (160.7 ± 52 mg/dL) (p=0.013). However, no statistically significant difference was observed between the groups in terms of HbA1c level. Proteinuria levels were higher in hypomagnesemia group (0.18 ±0.12 mg/mg) than normomagnesemia group (0.14±0.05 mg/mg) (p=0.013). Magnesium deficiency is a common condition in diabetic patiens and may have negative effects on glucose regulation and proteinuria. Randomized controlled trials are needed to clarify the role of magnesium in diabetic complications.

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Low extracellular magnesium does not impair glucose-stimulated insulin secretion

Cited by 19 publications

References 24 publications

TRPM7 is a critical regulator of pancreatic endocrine development and high-fat diet-induced β-cell proliferation

TRPM7 is a critical regulator of pancreatic endocrine development and high-fat diet-induced β-cell proliferation

Molecular Regulations and Functions of the Transient Receptor Potential Channels of the Islets of Langerhans and Insulinoma Cells

The Relationship between Magnesium Level with Glucose Regulation and Amount of Proteinuria in Type 2 Diabetes

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