Metabolism–Secretion Coupling and Mitochondrial Calcium Activities in Clonal Pancreatic β-Cells

Groschner, Lukas N.; Alam, Muhammad Rizwan; Graier, Wolfgang F.

doi:10.1016/b978-0-12-800174-5.00003-x

Cited by 3 publications

(3 citation statements)

References 116 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this part of the review we will focus on the role of mitochondrial [Ca 2+ ] ([Ca 2+ ] mito ) in ␤-cells. Recent detailed reviews can also be found [23,[234][235][236][237][238].…”

Section: Ca 2+ Changes In ␤-Cell Mitochondria ([Ca 2+ ] M )mentioning

confidence: 98%

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

et al. 2014

View full text Add to dashboard Cite

“…In this part of the review we will focus on the role of mitochondrial [Ca 2+ ] ([Ca 2+ ] mito ) in ␤-cells. Recent detailed reviews can also be found [23,[234][235][236][237][238].…”

Section: Ca 2+ Changes In ␤-Cell Mitochondria ([Ca 2+ ] M )mentioning

confidence: 98%

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

et al. 2014

View full text Add to dashboard Cite

“…β-cell dysfunction or reduced mass leads to impaired glucose tolerance, type 2 diabetes and associated complications (Steffes et al, 2003;Weir and Bonner-Weir, 2004). Metabolism-secretion coupling describes the molecular mechanism linking nutrient sensing and signaling to insulin secretion (Groschner et al, 2014;Henquin, 2000). For glucose-stimulated insulin secretion this process has been relatively well characterized and requires the sequential activation of several biological processes (Fig.…”

Section: Introductionmentioning

confidence: 99%

A novel ATP-synthase-independent mechanism coupling mitochondrial activation to exocytosis in insulin-secreting cells

Marchi

Hermant

Thévenet

et al. 2017

Journal of Cell Science

View full text Add to dashboard Cite

Pancreatic β-cells sense glucose, promoting insulin secretion. Glucose sensing requires the sequential stimulation of glycolysis, mitochondrial metabolism and Ca entry. To elucidate how mitochondrial activation in β-cells contributes to insulin secretion, we compared the effects of glucose and the mitochondrial substrate methylsuccinate in the INS-1E insulin-secreting cell line at the respective concentrations at which they maximally activate mitochondrial respiration. Both substrates induced insulin secretion with distinct respiratory profiles, mitochondrial hyperpolarization, NADH production and ATP-to-ADP ratios. In contrast to glucose, methylsuccinate failed to induce large [Ca] rises and exocytosis proceeded largely independently of mitochondrial ATP synthesis. Both glucose- and methylsuccinate-induced secretion was blocked by diazoxide, indicating that Ca is required for exocytosis. Dynamic assessment of the redox state of mitochondrial thiols revealed a less marked reduction in response to methylsuccinate than with glucose. Our results demonstrate that insulin exocytosis can be promoted by two distinct mechanisms one of which is dependent on mitochondrial ATP synthesis and large Ca transients, and one of which is independent of mitochondrial ATP synthesis and relies on small Ca signals. We propose that the combined effects of Ca and redox reactions can trigger insulin secretion by these two mechanisms.

show abstract

“…Moreover, AITC may markedly increase formation of reactive oxygen species (ROS) [38]. Glucose-induced insulin secretion is strongly dependent on mitochondrial metabolism and ATP formation [39]. It is also known that pancreatic β-cells are very vulnerable to the ROSmediated oxidative damage, because of low activity of antioxidative defense mechanisms, compared with other kinds of cells [40].…”

Section: Discussionmentioning

confidence: 99%

Differentiated Effects of Allyl Isothiocyanate in Diabetic Rats: From Toxic to Beneficial Action

Okulicz

Hertig

Szkudelski

2021

Toxins

View full text Add to dashboard Cite

Allyl isothiocyanate (AITC), a constituent of Brassica family plants, has been reported to possess a high bioactivity in animal and human cells, showing ambiguous properties from adverse to beneficial ones. It was reported its genotoxic, carcinogenic, goitrogenic effects. On the other side, AITC has shown anti-cancer, cardioprotective, neuroprotective, and lately anti-obesity abilities. So far, its anti-diabetic effects are poorly explored. We tried to assess AITC action on carbohydrate, lipid and hormonal disorders in high fat diet-fed/streptozotocin diabetic rats. In this report, diabetic rats were treated intragastrically at doses 2.5, 5 and 25 mg/kg b.w./day of AITC for 2 weeks. Irrespectively of doses, AITC considerably lowered thyroid hormones (fT4, fT3), increased liver TG content, and also caused robust LDL-cholesterol and direct bilirubin concentration enhancement. Moreover, AITC at the highest dose caused pancreatic amylase and lipase drops and thyroid gland hypertrophy. AITC at 2.5 and 5 mg significantly reduced blood glucose levels along with robust beta-hydroxybutyric acid drop. Additionally, AITC at 5 mg improved insulin sensitivity (HOMA-IR index) in spite of reduced blood insulin. To conclude, despite amelioration of diabetic hyperglycemia by AITC, the adverse lipids and hormonal effects may exclude its use as a health-promoting compound in terms of anti-diabetic properties.

show abstract

Metabolism–Secretion Coupling and Mitochondrial Calcium Activities in Clonal Pancreatic β-Cells

Cited by 3 publications

References 116 publications

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

A novel ATP-synthase-independent mechanism coupling mitochondrial activation to exocytosis in insulin-secreting cells

Differentiated Effects of Allyl Isothiocyanate in Diabetic Rats: From Toxic to Beneficial Action

Contact Info

Product

Resources

About