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Hypoglycemic Effect of Electroacupuncture at ST25 Through Neural Regulation of the Pancreatic Intrinsic Nervous System.

Abstract
Electroacupuncture (EA) is considered to have potential antidiabetic effects; however, the role of the pancreatic intrinsic nervous system (PINS) in EA-induced amelioration of type 2 diabetes (T2DM) remains unclear. Therefore, we investigated whether EA at ST25 exerts any beneficial effects on insulin resistance (IR), inflammation severity, and pancreatic β cell function via the PINS in a rat model of a high-fat diet-streptozotocin (HFD/STZ)-induced diabetes. To this end, Sprague Dawley rats were fed with HFD to induce IR, followed by STZ (35 mg/kg, i.p.) injection to establish the T2DM model. After hyperglycemia was confirmed as fasting glucose level > 16.7 mmol/L, the rats were treated with EA (2 mA, 2/15 Hz) for the next 28 days. Model rats showed increased serum glucose, insulin, IR, and TNF-α levels with a concomitant decrease in β cell function. Microscopy examination of the pancreas revealed pathological changes in islets, which reverted to near-normal levels after EA at ST25. EA improved islet cell morphology by increasing islet area and reducing vacuolation. EA at ST25 decreased transient receptor potential vanilloid 1 (TRPV1) and increased substance P (SP) and calcitonin gene-related peptide (CGRP) expression. Subsequently, insulin secretion decreased and impaired pancreatic endocrine function was restored through the TRPV1 channel (SP/CGRP)-insulin circuit. EA increased choline acetyltransferase and neuropeptide Y expression and controlled inflammation. It also enhanced the cocaine and amphetamine-regulated transcript prepropeptide expression and promoted glucagon-like peptide-1 secretion. Additionally, the electrophysiological activity of PINS during acupuncture (2.71 ± 1.72 Hz) was significantly increased compared to the pre-acupuncture frequency (0.32 ± 0.37 Hz, P < 0.05). Thus, our study demonstrated the beneficial effect of EA on β cell dysfunction via the PINS in rat models of HFD-STZ-induced T2DM.
AuthorsTiancheng Xu, Zhi Yu, Yun Liu, Mengjiang Lu, Meirong Gong, Qian Li, Youbing Xia, Bin Xu
JournalMolecular neurobiology (Mol Neurobiol) Vol. 59 Issue 1 Pg. 703-716 (Jan 2022) ISSN: 1559-1182 [Electronic] United States
PMID34757591 (Publication Type: Journal Article)
Copyright© 2021. The Author(s).
Chemical References
  • Blood Glucose
  • Insulin
  • TRPV Cation Channels
  • Trpv1 protein, rat
  • Substance P
  • Calcitonin Gene-Related Peptide
Topics
  • Animals
  • Blood Glucose (metabolism)
  • Calcitonin Gene-Related Peptide (genetics, metabolism)
  • Diabetes Mellitus, Experimental (genetics, metabolism, therapy)
  • Electroacupuncture
  • Hypoglycemia
  • Inflammation (metabolism)
  • Insulin (blood)
  • Insulin Resistance (physiology)
  • Insulin-Secreting Cells (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Substance P (genetics, metabolism)
  • TRPV Cation Channels (genetics, metabolism)

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