Dimethyl sulfoxide acutely enhances regulated insulin secretion in the MIN6-K8 mouse insulinoma cell line

Carmean, Christopher M.; Zhao, Lidan; Landeche, Michael; Chellan, Bijoy; Sargis, Robert M.

doi:10.1007/s00418-021-01984-z

Cited by 1 publication

(1 citation statement)

References 21 publications

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“…Kemp and Habener, 2002, demonstrated that 0.5-2.5% DMSO significantly enhanced insulin secretion and insulin gene expression in the INS beta cell line, which could be through direct molecular interaction with downstream target of the glucagonlike peptide 1 (GLP-1) receptor signalling pathway in the beta cell [33]. A recent study reported that enhanced insulin secretion was observed in a mouse insulinoma model of pancreatic beta cell, MIN6-K8, when exposed to high glucose medium in association with enhanced calcium influx, suggesting that DMSO's mechanism of action is upstream of calcium-dependant insulin granule exocytosis [34]. These results also suggest that the observed increase in insulin levels in the vehicle control group in our study might be the effect of DMSO injection.…”

Section: Discussionmentioning

confidence: 99%

New Treatment for Type 2 Diabetes Mellitus Using a Novel Bipyrazole Compound

Alqudah

Qnais

Wedyan

et al. 2023

Cells

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2′,3,3,5′-Tetramethyl-4′-nitro-2′H-1,3′-bipyrazole (TMNB) is a novel bipyrazole compound with unknown therapeutic potential in diabetes mellitus. This study aims to investigate the anti-diabetic effects of TMNB in a high-fat diet and streptozotocin-(HFD/STZ)-induced rat model of type 2 diabetes mellitus (T2D). Rats were fed HFD, followed by a single low dose of STZ (40 mg/kg). HFD/STZ diabetic rats were treated orally with TMNB (10 mg/kg) or (200 mg/kg) metformin for 10 days before terminating the experiment and collecting plasma, soleus muscle, adipose tissue, and liver for further downstream analysis. TMNB reduced the elevated levels of serum glucose in diabetic rats compared to the vehicle control group (p < 0.001). TMNB abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control rats (p < 0.001). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the diabetic rats treated with TMNB compared to the vehicle controls. The skeletal muscle and adipose tissue protein contents of GLUT4 and AMPK were upregulated following treatment with TMNB (p < 0.001, < 0.01, respectively). TMNB was able to upregulate GLUT2 and AMPK protein expression in liver (p < 0.001, < 0.001, respectively). LDL, triglyceride, and cholesterol were reduced in diabetic rats treated with TMNB compared to the vehicle controls (p < 0.001, 0.01, respectively). TMNB reduced MDA and IL-6 levels (p < 0.001), and increased GSH level (p < 0.05) in diabetic rats compared to the vehicle controls. Conclusion: TMNB ameliorates insulin resistance, oxidative stress, and inflammation in a T2D model. TMNB could represent a promising therapeutic agent to treat T2D.

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Section: Discussionmentioning

confidence: 99%