Testosterone deficiency and non-alcoholic fatty liver disease in men with type 2 diabetes mellitus

Abstract

BACKGROUND: Current studies investigated diseases associated with testosterone (T) deficiency; however, data on the combination of non-alcoholic fatty liver disease (NAFLD) with hypogonadism and diabetes mellitus (DM) in men are extremely limited.
 AIMS: To evaluate the effects of hypogonadism on the formation and progression of NAFLD in men with type 2 DM.
 METHODS: The study included 90 men with type 2 DM [age 54 (4957) years]. Patients underwent clinical examinations, biochemical analysis (alanine aminotransferase (ALT), aspartate aminotransferase, gamma-glutamyl transpeptidase (GGTP), fasting glucose, immunoreactive insulin, HOMA index, HbA1c, lipid profile), immune enzyme analysis (luteinising hormone, total T, sex hormone binding globulin, resistin, adiponectin, leptin) and magnetic resonance imaging with liver fat fraction determination were performed. Patients were divided into two groups: 132 eugonadal patients and 258 men with newly diagnosed hypogonadism.
 RESULTS: Increased insulin resistance, hyperinsulinemia, hypertriglyceridemia were observed in men with hypogonadism compared to eugonadal patients. Along with biochemical signs of impaired liver function, such as an increase in liver enzyme concentrations of ALT by 24.5% (p = 0.02), GGTP by 60.5% (p = 0.001), de Rytis coefficient by 60.4% (p = 0.047), of men in the 2nd group, the liver fat fraction also increased, which together indicates NAFLD progression. The proton density of the liver fat fraction according to MRI was 4.12 [2.255.30] % in the 1st group and 10.30 [7.78; 14.44] % in the 2nd group (p=0.001). This was accompanied by an increase in fat production of resistin by 2 times and leptin by 12 times (p 0.001) in patients of group 2 compared to 1.
 CONCLUSIONS: The combination of type 2 DM with hypogonadism in men leads not only to deterioration of carbohydrate and lipid metabolism but also to disturbance of liver function: increased ALT, GGTP concentrations and liver fat. Increased secretion of leptin and resistin in the adipose tissue is assumed to be a pathogenetically associated with the development of carbohydrate and lipid metabolism disorders, NAFLD and T deficiency.

New opportunities for the correction of non-alcoholic fatty liver disease in men with type 2 diabetes mellitus and hypogonadism

“…Таким образом, общность патогенетических механизмов развития компонентов метаболического синдрома, дефицита Т и НАЖБП обозначила новое направление в изучении взаимного влияния данных состояний [13]. Так, было установлено, что у мужчин с СД2 и гипогонадизмом НАЖБП выражена более значимо, чем у эугонадных пациентов, и ассоциирована с развитием гиперинсулинемии, инсулинорезистентности, на-рушениями липидного обмена и дисфункцией жировой ткани [14]. Получив столь важные результаты, возможно предположить, что восстановление дефицита Т может позитивно повлиять на функцию печени.…”

“…Ранее нами было показано, что дефицит Т у мужчин с СД2 ассоциирован с ухудшением функции печени и прогрессией НАЖБП по сравнению с нормогонадными пациентами, что и послужило поводом для поиска путей патогенетической коррекции данных состояний [14].…”