Abstract
Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l‐Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l‐Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose‐supplemented hyperuricemic, l‐Carnitine‐treated hyperuricemic, and l‐Carnitine‐treated fructose‐supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA‐IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose‐supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l‐Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l‐Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l‐Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose‐induced hyperuricemia effects, through its anti‐inflammatory, antisteatotic, and antioxidant properties.
Highlights
Hyperuricemia, the deposition of urate crystals in the joints caused by high uric acid level in the blood (Wu et al, 2014), could result from either overproduction of uric acid (10% of hyperuricemic cases), or from lowered uric acid excretion (90% of cases), or both (Wolff, Cruz, Vanderman, & Brown, 2015)
Group; these parameters were significantly higher in concomitant fructose supplementation and hyperuricemia group and l‐Carnitine treatment to hyperuricemic rats compared to either control ones or hyperuricemic rats (p < .001 for each one)
They were significantly reduced in l‐Carnitine‐treated fructose‐supplemented hyperuricemic rats compared to its respective untreated rats (p < .05, p < .01, respectively)
Summary
Hyperuricemia, the deposition of urate crystals in the joints caused by high uric acid level in the blood (Wu et al, 2014), could result from either overproduction of uric acid (10% of hyperuricemic cases), or from lowered uric acid excretion (90% of cases), or both (Wolff, Cruz, Vanderman, & Brown, 2015). Hyperuricemia in adults could ensue when blood uric acid is more than 7 mg/dl in men and 6 mg/dl in women. This sex difference was linked to the uricosuric effect of estrogens in women (Mumford et al, 2013). The gene expressing uricase enzyme could be mutant in human, uric acid could be the final end product of both endogenous and exogenous purine catabolism (Mandal & Mount, 2015). It was found that metabolic syndrome could be affected by uric acid level (Srikanthan, Feyh, Visweshwar, Shapiro, & Sodhi, 2016). Serum uric acid was found to be higher in metabolic syndrome states, elevating the number of components of the metabolic syndrome (Silva et al, 2015)
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