Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2022) 81 RC14.8 | DOI: 10.1530/endoabs.81.RC14.8

University of Bari, Department of Emergency and Organ Transplantation, Bari, Italy


Hepatocytes are both insulin sensitive and the primary site for synthesis of SHBG. Thus, it is possible that a condition of hepatic insulin resistance may impair hepatic synthesis of SHBG. In this study, we assessed SHBG circulating levels after 30 days of a very low-calorie ketogenic diet (VLCKD) based on high-biological value protein preparations diet (ISOMED) and natural food in a cohort of insulin-resistant obese male subjects. Moreover, we investigated the effects of exposure of different concentrations of glucose (5.5 mM, 10 mM, 30 mM) and human insulin (HI, 100 nM) on SHBG protein levels and analyzed the expression levels of insulin receptor (InsRec) in the hepatoma cell line HepG2. Twenty-two patients (mean age 39.3 ± 11.7 years, mean BMI 38.2 ± 6.4 kg/m2) displayed fasting glycaemia within the normal range (77.5 ± 10.4 mg/dl), but elevated levels of insulin (29.3 ± 17.8 µIU/ml) and HOMA-IR (5.9 ± 3.7). Mean serum SHBG level was 20.3 ± 8.9 nmol/l at baseline. After VLCKD, a decrease of body weight (-9.3 ± 1.9 Kg), BMI (-3.0 ± 0.7 Kg/m2), and fat mass (-6.4 ± 2.1 kg) (P< 0.01) was observed. A significant increase in serum SHBG levels (+ 7.7 ± 10 nmol/l) was also achieved after VLCKD, with a change of smaller magnitude in high (+2.9) vs low (+12.4) insulin resistance subjects. Interestingly, basal insulinemia (ß -0.6, P<0.01) and HOMA-IR (ß -3.2, P<0.05) appeared as negative predictors of SHBG variation at day 30, independently of BMI. In vitro results showed that 96-h treatment of HepG2 with high glucose concentrations (10 mM and 30 mM) resulted in higher SHBG protein levels (2-fold and 7-fold, respectively) and InsRec expression (1,5-fold and 2-fold, respectively) as compared to normal (5 mM) glucose. Conversely, the co-incubation with HI for 96 h blunted the augmentation of SHBG observed in the absence of insulin (-40% at 10 mM of glucose; -32% at 30 mM of glucose). Likewise, co-incubation with HI resulted in reduced InsRec expression by -67% and -60%, at 10 mM and 30 mM glucose respectively, compared to the absence of insulin. Altogether, these results suggest that high insulin levels may counteract the induction of SHBG during weight loss. In vitro data show that high insulin levels may favor hepatic insulin resistance by inhibition of insulin receptor expression and impair SHBG expression.

Volume 81

European Congress of Endocrinology 2022

Milan, Italy
21 May 2022 - 24 May 2022

European Society of Endocrinology 

Browse other volumes

Article tools

My recent searches

No recent searches.