Relatively low sex hormone‐binding globulin concentration is a risk factor for hyperuricemia in middle‐aged Japanese men

Abstract

Summary Objective Low testosterone and hyperuricemia are associated with metabolic syndrome (MetS). However, little is known about the nature of the relationships between serum testosterone and sex hormone‐binding globulin (SHBG) concentrations, and hyperuricemia. Methods We evaluated the relationships between serum testosterone (calculated bioavailable testosterone [cbT], calculated free testosterone [cFT], SHBG, and total testosterone [TT]) and metabolic indices, including serum uric acid, in 363 Japanese males (mean age 51.1 ± 8.7 years) at routine health examinations. Results Participants with hyperuricemia (≥7.0 mg/dL) demonstrated lower adiponectin, cbT, cFT, SHBG, and TT, but a higher MetS prevalence and higher values of various MetS‐related parameters than those without hyperuricemia (<7.0 mg/dL). Binary regression analysis revealed that less than 52 nmol/L SHBG, less than 5.0 μg/mL serum adiponectin, greater than or equal to 7.0 g/dL total protein, and greater than or equal to 1.0 mg/dL creatinine were statistically significant risk factors for hyperuricemia. Receiver operating characteristic analysis confirmed that less than 46.5 nmol/L (area under the curve [AUC] = 0.645) SHBG and less than 3.68 μg/mL (AUC = 0.691) adiponectin concentrations were significant risk factors for hyperuricemia. Conclusions We provide evidence that low SHBG provides an important marker for hyperuricemia in middle‐aged Japanese men. This finding provides clinical evidence that low SHBG is closely associated with MetS, which is often accompanied with hyperuricemia.

Uric acid participating in female reproductive disorders: a review

“…SHBG can also bind free androgens to reduce their levels and control their bioavailability to indirectly affect the UA concentration. Fujihara et al [ 42 ] suggested that a lower concentration of SHBG (46.5 nmol/L) was a predictor of hyperuricaemia, which may lead to reduced production of SHBG via induced inactivation of AMPK in the liver [ 43 ].…”