Oral Presentation ANZOS Annual Scientific Meeting 2021

Associations of reproductive hormones and glucose homeostasis with metabolic-associated fatty liver disease measured by transient elastography in a super-obese population (#116)

Houston Xue 1 , Annette McDonald 2 , Amy Phu 3 , Ramy H Bishay 1 2 , Golo Ahlenstiel 1 3 4
  1. School of Medicine, Western Sydney University, Campbelltown, NSW, Australia
  2. Blacktown Metabolic and Weight Loss Program, Department of Endocrinology, Blacktown Hospital, Blacktown, NSW, Australia
  3. Storr Liver Centre, Westmead Millennium Institute, University of Sydney, Sydney, NSW, Australia
  4. Department of Gastro and Hepatology, Blacktown Hospital, Western Sydney Local Health District, Sydney, NSW, Australia

Introduction: Low sex hormone binding globulin (SHBG) has been associated with obesity and related metabolic diseases including metabolic-associated fatty liver disease (MAFLD) and type 2 diabetes mellitus (T2D), but no studies have examined the relative significance of these relationships with MAFLD diagnosed by transient elastography or in a super-obese community-based population.

Methods: Patients were prospectively recruited into an observational cohort study to the public Blacktown Hospital Metabolic and Weight Loss Program - a tertiary weight management service in Western Sydney. Patients were referred by their primary care physician if they had a BMI>35 kg/m2 with T2D or BMI>40 kg/mwith two obesity complications. Anthropometric measurements, metabolic and hormonal blood tests and transient elastography data were collected at baseline.

Results: The cohort comprised of 317 patients (48.9±13 yrs, 68% female, BMI 50.7±12 kg/m2). 87% had steatosis as defined by controlled attenuation parameter (CAP) >280dB/m on transient elastography (FibroScan®), and this was significantly associated with lower SHBG and higher HOMA2-IR in both genders, and higher BMI, waist circumference, glycosylated haemoglobin and triglycerides only in women. Addition of prediabetes/diabetes to steatosis did not significantly change the association with SHBG or HOMA2-IR. Lower SHBG correlated with higher CAP, glycosylated haemoglobin, HOMA2-IR and triglycerides in both genders, but not measures of adiposity including BMI or waist circumference, nor Edmonton Obesity stage. Controlling for SHBG did not modify the relationship of steatosis with any metabolic parameters apart from calculated free testosterone in women.

Conclusions: In our cohort of community-dwelling severe complex obesity, low SHBG was an adiposity-independent marker of metabolic health, especially aligning with steatosis. The relationships of steatosis with adiposity, glucose homeostasis and lipids were sex dimorphic and further research is needed to clarify these findings. Beyond a rise in free testosterone, low SHBG did not mediate the metabolic associations of steatosis in women.