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      Characterization of inflammation and insulin resistance in high‐fat diet‐induced male C57BL/6J mouse model of obesity

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          Abstract

          Background

          Animal models of diet‐induced obesity (DIO) are commonly used in medical research for mimicking human diseases. There is no universal animal model, and careful evaluation of variety of factors needs to be considered when designing new experiments. Here, we investigated the effect of 9 weeks high‐fat diet (HFD) intervention, providing 60% energy from fat, on parameters of inflammation and insulin resistance in male C57BL/6J mice.

          Methods

          Six weeks old mice were initiated on regular diet (RD) or HFD providing 60 kcal energy from fat for 9 weeks. Fasting blood glucose levels were measured by glucometer, and fasting plasma levels of insulin and proinflammatory cytokines by Luminex assay. Insulin sensitivity was evaluated by using QUICKI and HOMA2 indexes.

          Results

          HFD mice showed ~ 40% higher body weight and ~ 20% larger abdominal circumference, due to an increase in the white adipose tissue mass. Liver examination revealed increased size and higher hepatic lipid accumulation in livers from HFD mice compared to their RD counterparts. Animals from the HFD group were characterized with significantly higher presence of crown‐like structures (CLS) in WAT and higher plasma levels of proinflammatory cytokines (TNF‐α, IL‐6, leptin, MCP‐1, PAI‐1, and resistin). HFD‐fed mice also demonstrated impaired insulin sensitivity (lower QUICKI, higher HOMA‐insulin resistance (HOMA‐IR), and lower HOMA‐percent sensitivity (HOMA‐%S)) index values.

          Conclusion

          Male C57BL/6J mice on 9 weeks HFD providing 60 kcal energy from fat display impaired insulin sensitivity and chronic inflammation, thus making this DIO mouse model appropriate for studies of early stages of obesity‐related pathology.

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          Most cited references21

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          Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans.

          Insulin resistance plays an important role in the pathophysiology of diabetes and is associated with obesity and other cardiovascular risk factors. The "gold standard" glucose clamp and minimal model analysis are two established methods for determining insulin sensitivity in vivo, but neither is easily implemented in large studies. Thus, it is of interest to develop a simple, accurate method for assessing insulin sensitivity that is useful for clinical investigations. We performed both hyperinsulinemic isoglycemic glucose clamp and insulin-modified frequently sampled iv glucose tolerance tests on 28 nonobese, 13 obese, and 15 type 2 diabetic subjects. We obtained correlations between indexes of insulin sensitivity from glucose clamp studies (SI(Clamp)) and minimal model analysis (SI(MM)) that were comparable to previous reports (r = 0.57). We performed a sensitivity analysis on our data and discovered that physiological steady state values [i.e. fasting insulin (I(0)) and glucose (G(0))] contain critical information about insulin sensitivity. We defined a quantitative insulin sensitivity check index (QUICKI = 1/[log(I(0)) + log(G(0))]) that has substantially better correlation with SI(Clamp) (r = 0.78) than the correlation we observed between SI(MM) and SI(Clamp). Moreover, we observed a comparable overall correlation between QUICKI and SI(Clamp) in a totally independent group of 21 obese and 14 nonobese subjects from another institution. We conclude that QUICKI is an index of insulin sensitivity obtained from a fasting blood sample that may be useful for clinical research.
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            Adapting to obesity with adipose tissue inflammation

            Adipose tissue inflammation is an adaptive response to overnutrition in the early stages of obesity, but later becomes maladaptive. Here, Reilly and Saltiel review the cellular and molecular mechanisms of obesity-induced inflammation in adipose tissue and discuss potential therapeutic approaches.
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              High-fat diet-induced obesity in animal models.

              Epidemiological studies have shown a positive relationship between dietary fat intake and obesity. Since rats and mice show a similar relationship, they are considered an appropriate model for studying dietary obesity. The present paper describes the history of using high-fat diets to induce obesity in animals, aims to clarify the consequences of changing the amount and type of dietary fats on weight gain, body composition and adipose tissue cellularity, and explores the contribution of genetics and sex, as well as the biochemical basis and the roles of hormones such as leptin, insulin and ghrelin in animal models of dietary obesity. The major factors that contribute to dietary obesity - hyperphagia, energy density and post-ingestive effects of the dietary fat - are discussed. Other factors that affect dietary obesity including feeding rhythmicity, social factors and stress are highlighted. Finally, we comment on the reversibility of high-fat diet-induced obesity.
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                Author and article information

                Contributors
                davtanski@northwell.edu
                Journal
                Animal Model Exp Med
                Animal Model Exp Med
                10.1002/(ISSN)2576-2095
                AME2
                Animal Models and Experimental Medicine
                John Wiley and Sons Inc. (Hoboken )
                2096-5451
                2576-2095
                25 September 2019
                December 2019
                : 2
                : 4 ( doiID: 10.1002/ame2.v2.4 )
                : 252-258
                Affiliations
                [ 1 ] Lenox Hill Hospital Friedman Diabetes Institute Northwell Health New York NY USA
                [ 2 ] The Feinstein Institutes for Medical Research Northwell Health Manhasset NY USA
                [ 3 ] Donald and Barbara Zucker School of Medicine at Hofstra/Northwell Hempstead NY USA
                Author notes
                [*] [* ] Correspondence

                Dimiter Avtanski, Ph.D., Friedman Diabetes Institute, Northwell Health, 110 E 59th Street, Suite 8B, Room 837, New York, NY 10022, USA.

                Email: davtanski@ 123456northwell.edu

                Article
                AME212084
                10.1002/ame2.12084
                6930989
                27abf665-16fc-46fd-8777-8e41dbb723c0
                © 2019 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Page count
                Figures: 4, Tables: 3, Pages: 7, Words: 4031
                Product
                Funding
                Funded by: Gerald J. and Dorothy R. Friedman New York Foundation for Medical Research
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                December 2019
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.3 mode:remove_FC converted:26.12.2019

                diet,high‐fat,insulin resistance,mouse model
                diet, high‐fat, insulin resistance, mouse model

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