Event Abstract Back to Event Dexamethasone causes dose-dependent decrease in insulin sensitivity in Wistar albino rats Rajasekhar Chinta1*, Kokila B Nagaraju2, Raghu Jetti3 and NagendraNayak IM4 1 Manipal Academy of Higher Education, Department of Pharmacology, Melaka Manipal Medical College, India 2 KVG Medical College & Hospital, Department of Pharmacology, India 3 King Khalid University, Department of Basic Medical Sciences, College of Applied Medical Sciences, Saudi Arabia 4 Mount Zion Medical College Hospital, Department of Pharmacology, India Background Long term administration of dexamethasone induces adverse effects such as muscle catabolism, hyperplasia, increased adiposity, and insulin resistance (IR). In view of these data, many authors tried to induce IR with different individual dose ranges with varied induction period. In this study, dexamethasone was used to find the dose to induce maximum insulin resistance in rodents. Methods A sum of 42 healthy male Wistar albino rats were categorized into six groups of dexamethasone treatment and one control group (n=6/group). In a six-day study period, all treatment groups received respective graded doses of dexamethasone starting from low- (0.5mg/kg and 1mg/kg), intermediate- (2mg/kg and 4mg/kg) and high-dose (8mg/kg and 16mg/kg). Results Graded doses of dexamethasone treatment for six days produced hyperglycemia and hyperinsulinemia in a dose-dependent manner and the maximum effect was noted with high doses of dexamethasone compared to intermediate and low (p<0.05). The profound reduction in insulin sensitivity was caused by high-doses of dexamethasone treatment evidenced by sustained elevation of homeostatic model assessment of insulin resistance (HOMA-IR) which was strongly associated with declined homeostatic model assessment of insulin sensitivity (HOMA-IS), The peripheral sensitivity indices, Gutt and Matsuda, were markedly elevated in high dexamethasone groups compared to intermediate- and low-dose groups (p<0.05). Serum lipids and creatinine (p<0.05), whereas high density lipoprotein cholesterol (HDL-CH) was markedly reduced and resulted in the subsequent rise in atherogenic index (AGI) (p<0.05). Moderate to severe glycosuria and ketonuria were noted in intermediate- and high-dose treatment groups only. However, there is no significant difference in metabolic effects between 8mg/kg and 16mg/kg treatments (p>0.05). Conclusion Administration of 8mg/kg dexamethasone for six days would be sufficient for the induction of maximum insulin resistance in Wistar albino rats. Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 Figure 11 Image 1 Image 2 Keywords: HOMA, Insulin Resistance, Hyperglycemia, hyperinsulinemia, Metabolic effects Conference: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”, Putrajaya, Malaysia, 3 Dec - 5 Feb, 2019. Presentation Type: Poster Presentation Topic: Metabolic diseases Citation: Chinta R, B Nagaraju K, Jetti R and IM N (2019). Dexamethasone causes dose-dependent decrease in insulin sensitivity in Wistar albino rats. Front. Pharmacol. Conference Abstract: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”. doi: 10.3389/conf.fphar.2019.63.00014 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 30 Sep 2018; Published Online: 17 Jan 2019. * Correspondence: Dr. Rajasekhar Chinta, Manipal Academy of Higher Education, Department of Pharmacology, Melaka Manipal Medical College, Manipal, India, diya.chinta@manipal.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Rajasekhar Chinta Kokila B Nagaraju Raghu Jetti NagendraNayak IM Google Rajasekhar Chinta Kokila B Nagaraju Raghu Jetti NagendraNayak IM Google Scholar Rajasekhar Chinta Kokila B Nagaraju Raghu Jetti NagendraNayak IM PubMed Rajasekhar Chinta Kokila B Nagaraju Raghu Jetti NagendraNayak IM Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.