High Serum Uric Acid and Increased Risk of Type 2 Diabetes: A Systemic Review and Meta-Analysis of Prospective Cohort Studies

Lv, Qing; Meng, Xianhong; He, Fang-Fang; Chen, Shan; Su, Hua; Xiong, Jing; Gao, Pan; Tian, Xiujuan; Liu, Jianshe; Zhu, Zhaohui; Huang, Kai; Zhang, Chun

doi:10.1371/journal.pone.0056864

Cited by 286 publications

(237 citation statements)

References 35 publications

(56 reference statements)

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“…31 Our study results are consistent with that there was a significant rise in blood sugar levels as depicted in Tables 2 and 3. There are reported studies suggesting increased uric acid levels are associated with alteration in lipid levels and positively correlated to hypertriglyceridemia, hypercholesterolemia and increased arterial tone, whereas HDL levels were inversely correlated with serum uric acid levels. 32,33 In our study there was slight elevation triglycerides and total cholesterol but values were not statistically significant as compared to control group.…”

supporting

confidence: 92%

Evaluation of changes in rat fatigability and biochemical parameters after oral and intra-peritoneal administration of adenosine tri phosphate: an experimental study

Bannale

Kashinakunti

Manjula

et al. 2016

Int J Basic Clin Pharmacol

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supporting

confidence: 92%

Evaluation of changes in rat fatigability and biochemical parameters after oral and intra-peritoneal administration of adenosine tri phosphate: an experimental study

Bannale

Kashinakunti

Manjula

et al. 2016

Int J Basic Clin Pharmacol

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“…Sirota et al [33] revealed that increased serum uric acid levels are associated with greater severity of NAFLD by ultrasonography. Several prospective and retrospective studies have also provided evidences supporting the association of high serum uric acid, the risk of T2DM, cardiovascular diseases and hepatitis [34][35][36] . These have further supported that NAFLD is the hepatic manifestation of MetS.…”

Section: Metabolic Pathwaysmentioning

confidence: 93%

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Lim

Dillon

Miller

2014

WJG

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Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder that covers wide spectrum of liver pathology. NAFLD is strongly associated with liver inflammation, metabolic hyperlipidaemia and insulin resistance. Frequently, NAFLD has been considered as the hepatic manifestation of metabolic syndrome. The pathophysiology of NAFLD has not been fully elucidated. Some patients can remain in the stage of simple steatosis, which generally is a benign condition; whereas others can develop liver inflammation and progress into non-alcoholic steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. The mechanism behind the progression is still not fully understood. Much ongoing proteomic researches have focused on discovering the unbiased circulating biochemical markers to allow early detection and treatment of NAFLD. Comprehensive genomic studies have also begun to provide new insights into the gene polymorphism to understand patientdisease variations. Therefore, NAFLD is considered a complex and mutifactorial disease phenotype resulting from environmental exposures acting on a susceptible polygenic background. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. For proteomics section, this review highlighted functional proteins that involved in: (1) transportation; (2) metabolic pathway; (3) acute phase reaction; (4) antiinflammatory; (5) extracellular matrix; and (6) immune system. In the genomic studies, this review will discuss genes which involved in: (1) lipolysis; (2) adipokines; and (3) cytokines production. Key words: Non-alcoholic fatty liver disease; Proteomics; Genomics; Metabolic syndrome; Pathophysiology Core tip: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder in Western populations. NAFLD can occur as a spectrum diseases, from simple steatosis, to non-alcoholic steatohepatitis characterised by hepatocellular injury and inflammation, to cirrhosis and hepatocellular carcinoma. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. This review highlighted several functional proteins and genetic polymoprhisms; particular those involved in insulin resistance, triglycerides metabolism and hepatic inflammation. It is hoped that this review will offer further insights into the pathophysiology of NAFLD.

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“…Since NAFLD is a hepatic manifestation closely related to elevated levels of SUA and insulin resistance, this association has been studied in several studies among T2DM subjects. 12,13 Compared with non diabetic subjects, T2DM are believed to have an increased risk of developing NAFLD, but the true prevalence of the disorder among prediabetic subjects has not been systematically assessed. In addition, so far, population-based data to determine whether SUA and insulin resistance levels are associated with NAFLD in different stages of impaired glucose regulation, in particular prediabetic states, is scarce.…”

Section: Introductionmentioning

confidence: 99%

Elevated levels of serum uric acid and insulin resistance are associated with nonalcoholic fatty liver disease among prediabetic subjects

Hossain¹

2016

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Background: Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of insulin resistance and serum uric acid (SUA) levels seemed to be elevated during this disorder. There is a paucity of data regarding the association of SUA with NAFLD in prediabetes. In this context, the present study has been undertaken to investigate this association. Methods: In a cross-sectional analytical design, a total of 110 prediabetic subjects [M/F; 63/47, age in ranges, 45 (25-68)] were recruited in the study and divided into non NAFLD (n = 62) and NAFLD (n = 48) group after examined with ultrasonogram. Insulin resistance (HOMA-IR) was calculated by homeostasis model assessment. Results: NAFLD subjects had significantly higher levels of SUA compared to non NAFLD subjects (6.10 ± 1.42 vs. 5.38 ± 1.14, p = 0.004). They also had significantly higher levels of HOMA-IR (2.4 ± 1.09 vs. 1.4 ± 0.45, p < 0.001). In binary logistic regression analysis, HbA1c (OR = 3.505, p = 0.002), SUA (OR = 1.514, p = 0.023) and HOMA-IR (OR = 1.478, p = 0.029) were found to be significant determinants of NAFLD after adjusting the effects of BMI and triglyceride (TG). In multiple linear regression analysis, SUA showed significant positive association with HOMA-IR (ß = 0.355, p = 0.027) and TG (ß = 0.325, p = 0.033) after adjusting the effects of BMI and HbA1c. Conclusions: Increased levels of serum uric acid are significantly associated with NAFLD and this association seemed to be mediated by insulin resistance among prediabetic subjects.

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High Serum Uric Acid and Increased Risk of Type 2 Diabetes: A Systemic Review and Meta-Analysis of Prospective Cohort Studies

Cited by 286 publications

References 35 publications

Evaluation of changes in rat fatigability and biochemical parameters after oral and intra-peritoneal administration of adenosine tri phosphate: an experimental study

Evaluation of changes in rat fatigability and biochemical parameters after oral and intra-peritoneal administration of adenosine tri phosphate: an experimental study

Proteomic and genomic studies of non-alcoholic fatty liver disease - clues in the pathogenesis

Elevated levels of serum uric acid and insulin resistance are associated with nonalcoholic fatty liver disease among prediabetic subjects

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