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      Serum Uric Acid and Diabetes: From Pathophysiology to Cardiovascular Disease

      Author(s): 1 , 2 , 3
      Publication date Created:
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      Journal: Current Pharmaceutical Design
      Publisher: Bentham Science Publishers Ltd.

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          Abstract

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          Hyperuricemia, has been traditionally related to nephrolithiasis and gout. However, it has also been associated with the development of type 2 diabetes mellitus (T2DM) and cardiometabolic and cardiovascular diseases. Pathophysiologically, elevated serum uric acid (SUA) levels may be associated with abnormal lipid and glucose metabolism.

          :

          In this narrative review, we consider the associations between hyperuricemia, hyperglycemia, atherosclerosis and thrombosis. Furthermore, we comment on the available evidence linking elevated SUA levels with the incidence and outcomes of coronary heart disease, stroke, peripheral artery disease and non-alcoholic fatty liver in subjects with T2DM. The effects of antidiabetic drugs (e.g. metformin, pioglitazone, sulfonylureas, dipeptidyl peptidase 4 inhibitors, glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter 2 inhibitors and insulin) on SUA concentrations are also reviewed.

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          Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement

          Ian Neeland, Robert Ross, Jean-Pierre Després … (2019)
          Findings from epidemiological studies over the past 30 years have shown that visceral adipose tissue, accurately measured by CT or MRI, is an independent risk marker of cardiovascular and metabolic morbidity and mortality. Emerging evidence also suggests that ectopic fat deposition, including hepatic and epicardial fat, might contribute to increased atherosclerosis and cardiometabolic risk. This joint position statement from the International Atherosclerosis Society and the International Chair on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral adiposity and ectopic fat as emerging risk factors for type 2 diabetes, atherosclerosis, and cardiovascular disease, with a focus on practical recommendations for health professionals and future directions for research and clinical practice. We discuss the measurement of visceral and ectopic fat, pathophysiology and contribution to adverse health outcomes, response to treatment, and lessons from a public health programme targeting visceral and ectopic fat. We identify knowledge gaps and note the need to develop simple, clinically applicable tools to be able to monitor changes in visceral and ectopic fat over time. Finally, we recognise the need for public health messaging to focus on visceral and ectopic fat in addition to excess bodyweight to better combat the growing epidemic of obesity worldwide.
          Article 0 comments Cited 382 times – based on 0 reviews     Review now
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            A causal role for uric acid in fructose-induced metabolic syndrome.

            Takahiko Nakagawa, Hanbo Hu, Sergey Zharikov … (2006)
            The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.
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              How Does Empagliflozin Reduce Cardiovascular Mortality? Insights From a Mediation Analysis of the EMPA-REG OUTCOME Trial

              Silvio E Inzucchi, Bernard Zinman, David Fitchett … (2018)
              In the BI 10773 (Empagliflozin) Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG OUTCOME) trial involving 7,020 patients with type 2 diabetes and established cardiovascular (CV) disease, empagliflozin given in addition to standard of care reduced the risk of CV death by 38% versus placebo (hazard ratio [HR] 0.62 [95% CI 0.49, 0.77]). This exploratory mediation analysis assesses the extent to which treatment group differences in covariates during the trial contributed to CV death risk reduction with empagliflozin.
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                Author and article information

                Contributors
                Niki Katsiki: (View ORCID Profile)
                George D. Dimitriadis: (View ORCID Profile)
                Dimitri P. Mikhailidis: (View ORCID Profile)
                Journal
                Title: Current Pharmaceutical Design
                Abbreviated Title: CPD
                Publisher: Bentham Science Publishers Ltd.
                ISSN (Print): 13816128
                Publication date Created: May 2021
                Publication date (Print): May 2021
                Volume: 27
                Issue: 16
                Pages: 1941-1951
                Affiliations
                [1 ]First Department of Internal Medicine, Diabetes Center, Division of Endocrinology and Metabolism, AHEPA University Hospital, Thessaloniki,Greece
                [2 ]National and Kapodistrian University of Athens Medical School, Athens,Greece
                [3 ]Department of Clinical Biochemistry, Royal Free Hospital campus, University College London Medical School, University College London (UCL), London NW3 2QG,United Kingdom
                Article
                DOI: 10.2174/1381612827666210104124320
                PubMed ID: 33397230
                SO-VID: 47e12a56-9864-4f22-a298-b586a8ea3dac
                Copyright © © 2021
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