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      Acute effect of electroacupuncture at the Zusanli acupoints on decreasing insulin resistance as shown by lowering plasma free fatty acid levels in steroid-background male rats

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          Abstract

          Background

          Insulin sensitivity has been enhanced by electroacupuncture (EA) in rats, but the EA phenomenon in an insulin resistant state is still unclear. This study reports the use of a large dose of prednisolone to evaluate the effects of EA in a state of insulin resistance.

          Methods

          The plasma levels of free fatty acids (FFAs) were estimated in steroid-background rats (SBRs) and compared with those in healthy rats treated with normal saline. In addition, plasma glucose and endogenous insulin levels were assayed to calculate the homeostasis model assessment (HOMA) index. Intravenous glucose tolerance test (IVGTT) was carried out to compare glucose tolerance. The SBRs were randomly divided into EA-treatment and non-EA treatment groups and 15-Hz EA was applied to the bilateral Zusanli acupoints to investigate its effects on insulin resistance. In addition to an insulin challenge test (ICT) and IVGTT, the plasma levels of FFAs were measured and western blot was performed to help determine the effects of EA on the insulin resistant state.

          Results

          The plasma levels of FFAs increased markedly in SBRs, the HOMA index was markedly higher, and glucose tolerance was impaired. EA improved glucose tolerance and insulin sensitivity by decreasing the plasma levels of FFAs. Further, the insulin signaling proteins (IRS1) and glucose transporter isoform protein (GLUT4) in skeletal muscle inhibited by prednisolone recovered after EA.

          Conclusion

          Insulin resistance was successfully induced by a large dose of prednisolone in male rats. This insulin resistance can be improved by 15 Hz EA at the bilateral Zusanli acupoints, as shown by decreased plasma levels of FFAs.

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          Most cited references28

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          Phosphatidylinositol 3-kinase activation is required for insulin stimulation of pp70 S6 kinase, DNA synthesis, and glucose transporter translocation.

          J Blenis, Valerie C Kahn, Melvin L. Cheatham … (1994)
          Phosphatidylinositol 3-kinase (PI 3-kinase) is stimulated by insulin and a variety of growth factors, but its exact role in signal transduction remains unclear. We have used a novel, highly specific inhibitor of PT 3-kinase to dissect the role of this enzyme in insulin action. Treatment of intact 3T3-L1 adipocytes with LY294002 produced a dose-dependent inhibition of insulin-stimulated PI 3-kinase (50% inhibitory concentration, 6 microM) with > 95% reduction in the levels of phosphatidylinositol-3,4,5-trisphosphate without changes in the levels of phosphatidylinositol-4-monophosphate or its derivatives. In parallel, there was a complete inhibition of insulin-stimulated phosphorylation and activation of pp70 S6 kinase. Inhibition of PI 3-kinase also effectively blocked insulin- and serum-stimulated DNA synthesis and insulin-stimulated glucose uptake by inhibiting translocation of GLUT 4 glucose transporters to the plasma membrane. By contrast, LY294002 had no effect on insulin stimulation of mitogen-activated protein kinase or pp90 S6 kinase. Thus, activation of PI 3-kinase plays a critical role in mammalian cells and is required for activation of pp70 S6 kinase and DNA synthesis and certain forms of intracellular vesicular trafficking but not mitogen-activated protein kinase or pp90 S6 kinase activation. These data suggest that PI 3-kinase is not only an important component but also a point of divergence in the insulin signaling network.
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            The insulin signalling system and the IRS proteins.

            Megan M. White (1997)
            During the past few years, the insulin signalling system has emerged as a flexible network of interacting proteins. By utilizing the insulin receptor substrate (IRS)-proteins (IRS-1 and IRS-2), the insulin signal can be amplified or attenuated independently of insulin binding and tyrosine kinase activity, providing an extensible mechanism for signal transmission in multiple cellular backgrounds. By employing IRS-proteins to engage various signalling proteins, the insulin receptor avoids the stoichiometric constraints encountered by receptors which directly recruit SH2-proteins to their autophosphorylation sites. Finally, the shared use of IRS-proteins by multiple receptors is likely to reveal important connections between insulin and other hormones and cytokines which were previously unrecognized, or observed but unexplained.
            Article 0 comments Cited 66 times – based on 0 reviews     Review now
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              Analgesia induced by electroacupuncture of different frequencies is mediated by different types of opioid receptors: another cross-tolerance study.

              Xiao-Hong Chen, Ji-Sheng Han (1992)
              The cross-tolerance technique was used to analyze the receptor mechanisms of analgesia induced by electroacupuncture (EA) of 2 Hz, 100 Hz, or 2-15 Hz. (1) Rats were given EA stimulation of 2 Hz, 100 Hz and 2-15 Hz for 30 min with 30 min intervals successively. The percentage increase in tail-flick latency (TFL) was taken to indicate the intensity of EA analgesia. Rats made tolerant to repeated intrathecal injection of the mu-opioid agonist ohmefentanyl (OMF, 15 pmol, Q2h x 5) or the delta-opioid agonist DPDPE (10 nmol, Q2h x 5) showed a cross tolerance to both 2 Hz- and 2-15 Hz-, but not to 100 Hz-EA analgesia; and rats made tolerant to kappa-opioid agonist dynorphin-(1-13) (5 nmol, Q2h x 5) showed a cross-tolerance to 100 Hz- and 2-15 Hz-, but not to 2 Hz-EA analgesia; (2) Rats made tolerant to 2-15 Hz EA showed cross-tolerance to either 2 Hz- or 100 Hz-EA analgesia; (3) Rats made tolerant to either 2 Hz- or 100 Hz-EA were still reactive to 2-15 Hz-EA. The results indicate that 2 Hz-EA analgesia is mediated by mu- and delta-receptors, 100 Hz-EA analgesia by kappa-receptor, and 2-15 Hz-EA analgesia by combined action of mu-, delta- and kappa-receptors in the spinal cord of the rats.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMC Complement Altern Med
                Title: BMC Complementary and Alternative Medicine
                Publisher: BioMed Central
                ISSN (Electronic): 1472-6882
                Publication date Collection: 2009
                Publication date (Electronic): 1 August 2009
                Volume: 9
                Page: 26
                Affiliations
                [1 ]Department of Internal Medicine, Division of Endocrinology and Metabolism, Tungs' Taichung Metro Harbor Hospital, Taichung County, Taiwan, Republic of China
                [2 ]Department of Orthopedics, Taichung Veterans General Hospital, Taichung City, Taiwan, Republic of China
                [3 ]Department of Acupuncture, China Medical University Hospital, Taichung City, Taiwan, Republic of China
                [4 ]Department of Medicinal Botanicals and Health Care, Da-Yeh University, Chunghwa County, Taiwan, Republic of China
                [5 ]Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan, Republic of China
                [6 ]Graduate Institute of Chinese Medical Science, China Medical University, Taichung City, Taiwan, Republic of China
                [7 ]School of Chinese Medical Science, China Medical University, Taichung City, Taiwan, Republic of China
                Article
                Publisher ID: 1472-6882-9-26
                DOI: 10.1186/1472-6882-9-26
                PMC ID: 2731038
                PubMed ID: 19646276
                SO-VID: 27501769-77d7-464d-b766-f74282e93599
                Copyright © Copyright © 2009 Lin et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 April 2009
                Date accepted : 1 August 2009
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Complementary & Alternative medicine
                Data availability:
                ScienceOpen disciplines: Complementary & Alternative medicine

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