[ Nutrition ]

The Relation between Serum Uric Acid and HbA1c Is Dependent upon Hyperinsulinemia in Patients with

We aimed to investigate the causal effect of circulating uric acid concentrations on type 2 diabetes risk. A. The amount of visceral fat area was greater and the amount of subcutaneous fat area was less in people with type 2 DM than that in the people with normal glucose tolerance [16]. We also observed that the ORs were substantially higher for MetS [OR 3.97, (95% confidence interval 2.58-6.13)] (P < 0.001 for trend) and PLQ [OR 2.71 (95% confidence interval 1.62-4.47)] (p = 0.013 for trend) in the highest serum uric acid quartile compared with those in the lowest quartile. Since existing preventive drug therapies fail to completely prevent kidney damage, an examination of the effect of UA lowering against initiation and progression of renal and vascular complications is therefore of the utmost importance. The genetic score raised uric acid by 17 µmol/L (95% CI 15, 18) per SD increase and explained 4% of uric acid variation. © 2013 Springer Science+Business Media New York. Lack of "independence," therefore, does not necessarily mean lack of "causality." The importance of separating "independence" from "causality" is nicely reviewed by Johnson et al[1]. Intensive glucose and blood pressure control have thus far failed to adequately curb this problem and therefore a major need for novel treatment approaches exists. Such results may be attributed to the limited number of participants which had insufficient statistical power to detect a slight effect of the common polymorphism in PPARGC1A on T2DM susceptibility. However, we found no significant relationship between uric acid and HbA1c by regression analysis after adjusting total insulin. Lancet 2010;375:2161–7. If the consortium can demonstrate that allopurinol is capable of halting or slowing down loss of kidney function in people with type 1 diabetes by lowering people's levels of serum uric acid, it would be a major breakthrough for persons with diabetes. Renal insufficiency is a kidney-related condition that can cause increased creatinine and uric acid levels. Factors associated with diabetic retinopathy in chinese patients with type 2 diabetes mellitus. There is also a sex-based difference in the impact of HCV infection on diabetes. Hyperuricemia and gout can also be associated with decreased kidney function. Introduction Diabetes mellitus is a clinical syndrome which is characterized by hyperglycaemia due to an absolute or a relative deficiency of insulin. Patients with hyperuricemia are at a significantly higher risk of progressing to type 2 diabetes [2, 3]. A large number of researchers have begun to consider uric acid as a serum indicator of glycometabolic disorders, because of a correlation between uric acid and glucose metabolism [4, 5]. This suggests that lowering serum uric acid concentrations in this way does not have beneficial CVD effects.

Rather, the relationship follows more of a bell curve. Uric acid levels rise with increasing blood glucose concentrations in the normal and prediabetes population. However, in type 2 diabetes patients, uric acid levels tend to decline with increasing blood glucose concentrations [6, 7]. The reasons for the inverse relationship between uric acid and blood glucose in type 2 diabetes mellitus remain unclear. However, insulin levels are also closely related to uric acid levels. Serum uric acid levels will increase with increasing serum insulin levels in diabetic patients [8, 9]. Whether insulin is the factor that influences the relationship between the uric acid and blood glucose is not clear.

Previous studies did not provide an explanation. Thus, our study aimed to further explore the connection between uric acid and blood glucose in newly diagnosed type 2 diabetes. We performed a retrospective analysis on the inpatient database in the First Affiliated Hospital of Nanjing Medical University (China) between 2008 and 2014. We chose 605 individuals (435 males and 170 females) aged 30–74-years with newly diagnosed type 2 diabetes. The diagnosis for type 2 diabetes was in accordance with the diagnostic criteria promulgated by the World Health Organization (WHO) in 1990. Screening criteria were as follows: (1) patients must have newly diagnosed type 2 diabetes and have never received hypoglycemic drugs, diet, or exercise therapy prior to admission to the hospital. (2) Patients must have never received any drugs that would affect blood glucose, insulin, or serum uric acid before testing.

(3) Patients must have no history of serious liver or kidney problems or infection, trauma, or stress. Each RR was transformed into its nature logarithm value (logRR) and its corresponding 95% CI was used to calculate the logRR’s standard error (selogRR). There was no stress hyperglycemia or transient hyperglycemia caused by other reasons. There were 800 cases that were evaluated. Among them, 58 patients were excluded because they had taken drugs affecting uric acid, while 89 cases were excluded because they had impaired liver or kidney functions and 48 were not included because their data were incomplete. We analyzed the age, history of diabetes, height, weight, systolic blood pressure (SBP), and diastolic blood pressure (DBP) in all the patients. Nevertheless, there are limitations with using epidemiology to address causality, as the underlying premise is that the linkage between the factor and the outcome is direct.

The serology indexes, such as triglyceride (TG), creatinine (Cr), and serum uric acid (SUA) levels, were measured by automatic biochemical analyzer. Glycated hemoglobin (HbA1c) was measured by high-performance liquid chromatography (HPLC). Strasak AM, Rapp K, Hilbe W, Oberaigner W, Ruttmann E, Concin H, . Blood samples were collected at fasting (0 min) and at 30, 60, and 120 minutes after taking 75 g anhydrous glucose to measure plasma glucose (dextrose oxidase method) and serum insulin (radioimmunoassay). The body mass index (BMI) was calculated by dividing the weight (kg) by the height (m) squared. Total insulin level was represented as the area under curve of insulin during 0–120 min of the IRT [10], which was obtained from the irregular trapezoid method ( [11].

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