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      What is the relationship between serum uric acid level and insulin resistance?: A case-control study

      , Spec.MD a , * , , , Spec.MD b , , Spec.MD b
      Lippincott Williams & Wilkins
      cholesterol, HDL, insulin resistance, triglycerides, uric acid

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          Diabetes, arises from either an absolute or relative insufficiency of insulin or insulin resistance of peripheral tissues. For assessing long-term blood glucose concentration and insulin resistance, the utilization of glycosylated hemoglobin (HbA1c) and the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) is widespread. Insulin resistance can lead to hyperuricemia by reducing the kidney ability to excrete urate, thus increasing sodium reabsorption. The aim of this study was to investigate the possible relationship between serum uric acid levels and insulin resistance. This was a retrospective case-control study. A total of 2530 applications in 2-year time were included in the study. Patient, known hypertension status, fasting plasma glucose, insulin, uric acid, HDL, low-density lipoprotein (LDL), triglyceride/Tg, HbA1c laboratory values and Tg/HDL ratio were examined. A statistically significant difference existed in the median uric acid values between the insulin-resistant and insulin-sensitive groups ( P < .001). Additionally, a weak positive statistical correlation was identified between uric acid and HOMA-IR values ( R = 0.299; P < .001) and uric acid and Tg/HDL values ( R = 0.357; P < .001). This study concludes that there is a positive correlation between serum uric acid levels and insulin resistance.

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          Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage.

          Insulin resistance contributes to the pathophysiology of diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resistance in humans and animal models is of great importance for epidemiological studies, clinical and basic science investigations, and eventual use in clinical practice. Direct and indirect methods of varying complexity are currently employed for these purposes. Some methods rely on steady-state analysis of glucose and insulin, whereas others rely on dynamic testing. Each of these methods has distinct advantages and limitations. Thus, optimal choice and employment of a specific method depends on the nature of the studies being performed. Established direct methods for measuring insulin sensitivity in vivo are relatively complex. The hyperinsulinemic euglycemic glucose clamp and the insulin suppression test directly assess insulin-mediated glucose utilization under steady-state conditions that are both labor and time intensive. A slightly less complex indirect method relies on minimal model analysis of a frequently sampled intravenous glucose tolerance test. Finally, simple surrogate indexes for insulin sensitivity/resistance are available (e.g., QUICKI, HOMA, 1/insulin, Matusda index) that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or after an oral glucose load (dynamic). In particular, the quantitative insulin sensitivity check index (QUICKI) has been validated extensively against the reference standard glucose clamp method. QUICKI is a simple, robust, accurate, reproducible method that appropriately predicts changes in insulin sensitivity after therapeutic interventions as well as the onset of diabetes. In this Frontiers article, we highlight merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance.
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            High uric acid directly inhibits insulin signalling and induces insulin resistance.

            Accumulating clinical evidence suggests that hyperuricemia is strongly associated with abnormal glucose metabolism and insulin resistance. However, how high uric acid (HUA) level causes insulin resistance remains unclear. We aimed to determine the direct role of HUA in insulin resistance in vitro and in vivo in mice. An acute hyperuricemia mouse model was created by potassium oxonate treatment, and the impact of HUA level on insulin resistance was investigated by glucose tolerance test, insulin tolerance test and insulin signalling, including phosphorylation of insulin receptor substrate 1 (IRS1) and Akt. HepG2 cells were exposed to HUA treatment and N-acetylcysteine (NAC), reactive oxygen species scavenger; IRS1 and Akt phosphorylation was detected by Western blot analysis after insulin treatment. Hyperuricemic mice showed impaired glucose tolerance with insulin resistance. Hyperuricemia inhibited phospho-Akt (Ser473) response to insulin and increased phosphor-IRS1 (Ser307) in liver, muscle and fat tissues. HUA induced oxidative stress, and the antioxidant NAC blocked HUA-induced IRS1 activation and Akt inhibition in HepG2 cells. This study supplies the first evidence of HUA directly inducing insulin resistance in vivo and in vitro. Increased uric acid level may inhibit IRS1 and Akt insulin signalling and induce insulin resistance. The reactive oxygen species pathway plays a key role in HUA-induced insulin resistance. Copyright © 2014 Elsevier Inc. All rights reserved.
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              Molecular Biological and Clinical Understanding of the Pathophysiology and Treatments of Hyperuricemia and Its Association with Metabolic Syndrome, Cardiovascular Diseases and Chronic Kidney Disease.

              Uric acid (UA) is synthesized mainly in the liver, intestines, and vascular endothelium as the end product of an exogenous purine from food and endogenously from damaged, dying, and dead cells. The kidney plays a dominant role in UA excretion, and the kidney excretes approximately 70% of daily produced UA; the remaining 30% of UA is excreted from the intestine. When UA production exceeds UA excretion, hyperuricemia occurs. Hyperuricemia is significantly associated with the development and severity of the metabolic syndrome. The increased urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) expression, and glycolytic disturbances due to insulin resistance may be associated with the development of hyperuricemia in metabolic syndrome. Hyperuricemia was previously thought to be simply the cause of gout and gouty arthritis. Further, the hyperuricemia observed in patients with renal diseases was considered to be caused by UA underexcretion due to renal failure, and was not considered as an aggressive treatment target. The evidences obtained by basic science suggests a pathogenic role of hyperuricemia in the development of chronic kidney disease (CKD) and cardiovascular diseases (CVD), by inducing inflammation, endothelial dysfunction, proliferation of vascular smooth muscle cells, and activation of the renin-angiotensin system. Further, clinical evidences suggest that hyperuricemia is associated with the development of CVD and CKD. Further, accumulated data suggested that the UA-lowering treatments slower the progression of such diseases.

                Author and article information

                Medicine (Baltimore)
                Medicine (Baltimore)
                Lippincott Williams & Wilkins (Hagerstown, MD )
                29 December 2023
                29 December 2023
                : 102
                : 52
                : e36732
                [a ] Department of Family Medicine, Balikesir Atatürk City Hospital, Gaziosmanpaşa, Turkey
                [b ] Department of Family Medicine, Health Science University, Izmir Bozyaka Training and Education Hospital, Izmir, Turkey.
                Author notes
                [* ]Correspondence: Ayça Asma Sakalli, Balikesir Atatürk City Hospital, Gaziosmanpaşa, 209. Sk. No:26, Altieylül, Balikesir 10100, Turkey (e-mail: draycaasma@ 123456gmail.com ).
                Author information
                Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 04 September 2023
                : 28 November 2023
                : 29 November 2023
                Research Article
                Observational Study
                Custom metadata

                cholesterol,hdl,insulin resistance,triglycerides,uric acid
                cholesterol, hdl, insulin resistance, triglycerides, uric acid


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