Uric acid: from a biological advantage to a potential danger. A focus on cardiovascular effects

2019 ◽  
Vol 120 ◽  
pp. 106565 ◽  
Author(s):  
Francesca Cortese ◽  
Paola Giordano ◽  
Pietro Scicchitano ◽  
Maria Felicia Faienza ◽  
Giovanni De Pergola ◽  
...  
2018 ◽  
Vol 66 (7) ◽  
pp. 1037-1044
Author(s):  
Sun K Park ◽  
Tara R Rosenthal ◽  
Jessica S Williams ◽  
John M Shelton ◽  
Masaya Takahashi ◽  
...  

Mildly elevated serum uric acid levels are common in people with metabolic syndrome and type 2 diabetes mellitus (T2DM), but whether elevated uric acid has a causal role in the pathogenesis of diabetes remains uncertain. We tested whether chronic mild hyperuricemia in rodents under controlled laboratory conditions can cause glucose intolerance in otherwise healthy animals, or whether it can worsen glucometabolic control in animals that are genetically predisposed to T2DM. We used an established model of experimental hyperuricemia in rodents with potassium oxonate dietary supplementation, which led to sustained, approximately two-fold elevation of uric acid compared with control animals. We also reversed the hyperuricemic effect of oxonate in some animals by treatment with a xanthine oxidase inhibitor. Manipulation of serum uric acid levels in Sprague-Dawley rats for up to 18 weeks did not affect fasting glucose and glucose tolerance. Blood pressure was also not affected by hyperuricemia in rats fed a Western-type diet. We next sought to determine whether uric acid may aggravate or accelerate the onset of glucometabolic abnormalities in rats already predisposed to T2DM. Chronic oxonate treatment in Zucker diabetic fatty (ZDF) and lean control rats for up to 6 weeks did not affect fasting glucose, insulin, and glucose tolerance in ZDF rats. Taken together, these findings indicate that elevated uric acid does not directly contribute to the pathogenesis of glucose intolerance and T2DM in rodents.


2003 ◽  
Vol 2 (1) ◽  
pp. 79
Author(s):  
P PAVLIDIS ◽  
J PARISSIS ◽  
S ANTONOPOULOS ◽  
D POLLATOS ◽  
P KIRIAZOPOULOS ◽  
...  

JAMA ◽  
1966 ◽  
Vol 196 (4) ◽  
pp. 364-365 ◽  
Author(s):  
L. A. Healey
Keyword(s):  

Author(s):  
Sanem Kayhan ◽  
Nazli Gulsoy Kirnap ◽  
Mercan Tastemur

Abstract. Vitamin B12 deficiency may have indirect cardiovascular effects in addition to hematological and neuropsychiatric symptoms. It was shown that the monocyte count-to-high density lipoprotein cholesterol (HDL-C) ratio (MHR) is a novel cardiovascular marker. In this study, the aim was to evaluate whether MHR was high in patients with vitamin B12 deficiency and its relationship with cardiometabolic risk factors. The study included 128 patients diagnosed with vitamin B12 deficiency and 93 healthy controls. Patients with vitamin B12 deficiency had significantly higher systolic blood pressure (SBP), diastolic blood pressure (DBP), MHR, C-reactive protein (CRP) and uric acid levels compared with the controls (median 139 vs 115 mmHg, p < 0.001; 80 vs 70 mmHg, p < 0.001; 14.2 vs 9.5, p < 0.001; 10.2 vs 4 mg/dl p < 0.001; 6.68 vs 4.8 mg/dl, p < 0.001 respectively). The prevalence of left ventricular hypertrophy was higher in vitamin B12 deficiency group (43.8%) than the control group (8.6%) (p < 0.001). In vitamin B12 deficiency group, a positive correlation was detected between MHR and SBP, CRP and uric acid (p < 0.001 r:0.34, p < 0.001 r:0.30, p < 0.001 r:0.5, respectively) and a significant negative correlation was detected between MHR and T-CHOL, LDL, HDL and B12 (p < 0.001 r: −0.39, p < 0.001 r: −0.34, p < 0.001 r: −0.57, p < 0.04 r: −0.17, respectively). MHR was high in vitamin B12 deficiency group, and correlated with the cardiometabolic risk factors in this group, which were SBP, CRP, uric acid and HDL. In conclusion, MRH, which can be easily calculated in clinical practice, can be a useful marker to assess cardiovascular risk in patients with vitamin B12 deficiency.


VASA ◽  
2010 ◽  
Vol 39 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Grotenhermen

Background: To investigate the hypothesis that cases of arteritis similar to thromboangiitis obliterans (TAO) and associated with the use of cannabis were caused by cannabis or THC (dronabinol), or that cannabis use is a co-factor of TAO. Patients and methods: A systematic review on case reports and the literature on so-called cannabis arteritis, TAO, and cardiovascular effects of cannabinoids was conducted. Results: Fifteen reports with 57 cases of an arteritis associated with the use of cannabis and two additional case series of TAO, in which some patients also used cannabis, were identified. Clinical and pathological features of cannabis-associated arteritis do not differ from TAO and the major risk factor of TAO, tobacco use, was present in most, if not in all of these cases. The proposed pathophysiological mechanisms for the development of an arteritis by cannabis use are not substantiated. Conclusions: The hypothesis of cannabis being a causative factor or co-factor of TAO or an arteritis similar to TAO is not supported by the available evidence. The use of the term “cannabis arteritis” should be avoided until or unless more convincing scientific support is forthcoming.


1971 ◽  
Author(s):  
Leonard M. Zir ◽  
Robert T. Rubin ◽  
Richard H. Rahe ◽  
Ransom J. Arthur

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