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      Diabetes Mellitus, Nonalcoholic Fatty Liver Disease, and Conjugated Linoleic Acid (Omega 6): What Is the Link?

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          Abstract

          Background and Objective

          Type 2 DM and obesity are the coming epidemics and their association with NAFLD is well established; essential fatty acids are vital for body health yet the body cannot make them; 2 essential fatty acids are especially important: linoleic (omega-6) and alpha-linoleic (omega-3) acids; they can be considered as “bioactive lipids” and serve as functional foods.

          Methods

          50 type 2 Egyptian diabetic patients controlled on oral hypoglycemic drugs together with 20 age- and sex-matched healthy participants were enrolled in the study; all were subjected to complete history taking, BMI, fasting plasma glucose, HOMA-IR, ALT, AST, GGT, urea and creatinine, total lipid profile, hepatitis markers including hepatitis B surface antigen and hepatitis C virus antibodies, conjugated linoleic fatty acid “CLA,” and abdominal ultrasound for grading of NAFLD.

          Results

          Our study in Egyptian diabetics with NAFLD revealed a low level of serum CLA compared to healthy control; such deficiency was more marked with advanced grades of NAFLD; lowest levels were observed in those with severe steatosis (NASH) with definite association between CLA and obesity.

          Conclusion

          Insulin resistance is the main link between NAFLD, diabetes, and obesity. Conjugated linoleic acid (CLA) has a role in fat deposition in the liver and in development and improvement of insulin resistance. Fatty food had a documented role in the pathogenesis of obesity and diabetes but it can also be the cure.

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          Most cited references27

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          Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes.

          Nonalcoholic fatty liver disease (NAFLD), hepatic insulin resistance, and type 2 diabetes are all strongly associated and are all reaching epidemic proportions. Whether there is a causal link between NAFLD and hepatic insulin resistance is controversial. This review will discuss recent studies in both humans and animal models of NAFLD that have implicated increases in hepatic diacylglycerol (DAG) content leading to activation of novel protein kinase Cϵ (PKCϵ) resulting in decreased insulin signaling in the pathogenesis of NAFLD-associated hepatic insulin resistance and type 2 diabetes. The DAG-PKCϵ hypothesis can explain the occurrence of hepatic insulin resistance observed in most cases of NAFLD associated with obesity, lipodystrophy, and type 2 diabetes. © 2013 by the American Association for the Study of Liver Diseases.
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            Dietary sources of conjugated dienoic isomers of linoleic acid, a newly recognized class of anticarcinogens

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              Contribution of hepatic de novo lipogenesis and reesterification of plasma non esterified fatty acids to plasma triglyceride synthesis during non-alcoholic fatty liver disease.

              Non-alcoholic fatty liver disease (NAFLD) is frequently observed in insulin-resistant subjects and can lead to liver fibrosis and cirrhosis. The abnormalities of lipid metabolism behind this development of excess hepatic TG stores are poorly understood. To clarify these mechanisms we measured triglyceride secretion rate and the contributions of hepatic lipogenesis and reesterification of non-esterified fatty acids (NEFA) to this secretion in healthy subjects and in patients with clear evidence of NAFLD. All subjects were studied in the post-absorptive state. Hepatic lipogenesis was measured with deuterated water. NEFA turnover rate, triglyceride secretion rate and the contribution of NEFA reesterification to this secretion were determined with [1-(13)C] palmitate infusion. NAFLD patients had higher NEFA concentrations (p<0.05) but normal NEFA turnover rates (5.23 +/- 0.80 vs 5.91 +/- 0.97 micromol.kg(-1).min(-1) in control subjects, ns). Despite a trend for higher plasma triglyceride levels in patients (p<0.10), triglyceride turnover rates were not increased (0.11 +/- 0.01 micromol.kg(-1).min(-1) in patients vs 0.14 +/- 0.01 in controls, ns). However the contribution of hepatic lipogenesis to triglyceride secretion was largely increased in patients (14.9 +/- 2.7 vs 4.6 +/- 1.1% p<0.01) while that of NEFA reesterification was reduced (25.1 +/- 2.9 vs 52.8 +/- 6.2% p<0.01). Enhanced lipogenesis appears as a major abnormality of hepatic fatty metabolism in subjects with NAFLD. Therapeutic measures aimed at decreasing hepatic lipogenesis would therefore be the most appropriate in order to reduce hepatic TG synthesis and content in such patients.
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                Author and article information

                Contributors
                Journal
                J Diabetes Res
                J Diabetes Res
                JDR
                Journal of Diabetes Research
                Hindawi
                2314-6745
                2314-6753
                2019
                8 April 2019
                : 2019
                : 5267025
                Affiliations
                1Internal Medicine Department, Faculty of Medicine, Cairo University, Egypt
                2Biochemistry Department, Faculty of Medicine, Cairo University, Egypt
                Author notes

                Academic Editor: Antonio Brunetti

                Author information
                http://orcid.org/0000-0003-2450-808X
                Article
                10.1155/2019/5267025
                6476070
                31089474
                ee831eb7-6e2f-442e-8820-b715cef63b43
                Copyright © 2019 Mona Hegazy et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 7 July 2018
                : 5 March 2019
                : 18 March 2019
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                Research Article

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