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      Therapeutic Effect of P-Cymene on Lipid Profile, Liver Enzyme, and Akt/Mtor Pathway in Streptozotocin-Induced Diabetes Mellitus in Wistar Rats

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          Abstract

          Diabetes is a serious public health problem in low- and middle-income countries. There is a strong link between hyperglycemia, oxidative stress, inflammation, and the development of diabetes mellitus. PI3K/Akt/mTOR is the main signaling pathway of insulin for controlling lipid and glucose metabolism. P-cymene is an aromatic monoterpene with a widespread range of therapeutic properties including antioxidant and anti-inflammatory activity. In the present study, the antidiabetic effects of p-cymene were investigated. Diabetes was induced using streptozotocin in male Wistar rats. The effects of p-cymene and metformin were studied on levels of glucose (Glu), lipid profile, liver enzymes, oxidative stress, and the expression of Akt, phospho-Akt, and mTOR (mammalian target of rapamycin) proteins, using biochemical, histological, and immunohistochemical analysis. Data have shown that p-cymene can improve serum levels of Glu, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), and the expression of mTOR, Akt, and phospho-Akt protein in diabetic animals. These results suggest that p-cymene has hypoglycemia, hypolipidemia, and antioxidant properties. It can regulate Akt/mTOR pathway and reduce hepatic and pancreas injury. It can be suggested for diabetes management alone or simultaneously with metformin.

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          Most cited references53

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          mTOR signaling in growth control and disease.

          The mechanistic target of rapamycin (mTOR) signaling pathway senses and integrates a variety of environmental cues to regulate organismal growth and homeostasis. The pathway regulates many major cellular processes and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration. Here, we review recent advances in our understanding of the mTOR pathway and its role in health, disease, and aging. We further discuss pharmacological approaches to treat human pathologies linked to mTOR deregulation. Copyright © 2012 Elsevier Inc. All rights reserved.
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            10-year follow-up of intensive glucose control in type 2 diabetes.

            During the United Kingdom Prospective Diabetes Study (UKPDS), patients with type 2 diabetes mellitus who received intensive glucose therapy had a lower risk of microvascular complications than did those receiving conventional dietary therapy. We conducted post-trial monitoring to determine whether this improved glucose control persisted and whether such therapy had a long-term effect on macrovascular outcomes. Of 5102 patients with newly diagnosed type 2 diabetes, 4209 were randomly assigned to receive either conventional therapy (dietary restriction) or intensive therapy (either sulfonylurea or insulin or, in overweight patients, metformin) for glucose control. In post-trial monitoring, 3277 patients were asked to attend annual UKPDS clinics for 5 years, but no attempts were made to maintain their previously assigned therapies. Annual questionnaires were used to follow patients who were unable to attend the clinics, and all patients in years 6 to 10 were assessed through questionnaires. We examined seven prespecified aggregate clinical outcomes from the UKPDS on an intention-to-treat basis, according to previous randomization categories. Between-group differences in glycated hemoglobin levels were lost after the first year. In the sulfonylurea-insulin group, relative reductions in risk persisted at 10 years for any diabetes-related end point (9%, P=0.04) and microvascular disease (24%, P=0.001), and risk reductions for myocardial infarction (15%, P=0.01) and death from any cause (13%, P=0.007) emerged over time, as more events occurred. In the metformin group, significant risk reductions persisted for any diabetes-related end point (21%, P=0.01), myocardial infarction (33%, P=0.005), and death from any cause (27%, P=0.002). Despite an early loss of glycemic differences, a continued reduction in microvascular risk and emergent risk reductions for myocardial infarction and death from any cause were observed during 10 years of post-trial follow-up. A continued benefit after metformin therapy was evident among overweight patients. (UKPDS 80; Current Controlled Trials number, ISRCTN75451837.) 2008 Massachusetts Medical Society
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              Oxidative stress and diabetic complications.

              Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells of both large and small vessels, as well as in the myocardium. This increased superoxide production causes the activation of 5 major pathways involved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanced glycation end products), increased expression of the receptor for AGEs and its activating ligands, activation of protein kinase C isoforms, and overactivity of the hexosamine pathway. It also directly inactivates 2 critical antiatherosclerotic enzymes, endothelial nitric oxide synthase and prostacyclin synthase. Through these pathways, increased intracellular reactive oxygen species (ROS) cause defective angiogenesis in response to ischemia, activate a number of proinflammatory pathways, and cause long-lasting epigenetic changes that drive persistent expression of proinflammatory genes after glycemia is normalized ("hyperglycemic memory"). Atherosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS. Overexpression of superoxide dismutase in transgenic diabetic mice prevents diabetic retinopathy, nephropathy, and cardiomyopathy. The aim of this review is to highlight advances in understanding the role of metabolite-generated ROS in the development of diabetic complications.
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                Author and article information

                Contributors
                Journal
                J Obes
                J Obes
                JOBE
                Journal of Obesity
                Hindawi
                2090-0708
                2090-0716
                2022
                26 April 2022
                : 2022
                : 1015669
                Affiliations
                1Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
                2A & S Research Institute, Ministry of Science Research and Technology, Tehran, Iran
                Author notes

                Academic Editor: David H. St-Pierre

                Author information
                https://orcid.org/0000-0002-2479-5034
                https://orcid.org/0000-0001-9888-6935
                https://orcid.org/0000-0001-9211-5953
                https://orcid.org/0000-0002-5942-5770
                Article
                10.1155/2022/1015669
                9072059
                500e4a8e-455a-4ea7-913d-5b54d25d8ed4
                Copyright © 2022 Maryam Arabloei Sani 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
                : 23 May 2021
                : 28 September 2021
                : 12 April 2022
                Funding
                Funded by: Islamic Azad University
                Categories
                Research Article

                Nutrition & Dietetics
                Nutrition & Dietetics

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