Male and female ER-α knockout mice exhibit hepatic steatosis by increasing gene expression of lipogenic transcription factors such as sterol regulatory element binding protein 1c (SREBP-1c) and decreasing lipid transport genes 42, 43. We also found a close positive correlation between AR and the mRNA expression of several liver genes that participate in the regulation of lipid and glucose metabolism (Table 4). Thus, the increased insulin resistance in liver owing to testosterone treatment does not worsen T2DM condition, instead improves glucose homeostasis in the Treated animals. Thus, in our study, we infer that despite increased hepatic insulin resistance, PI3K-AKT-independent inhibition of GSK3α has reduced PEPCK level, and hence, hepatic gluconeogenesis in the liver of Treated animals.
Consuming high-GI carbohydrates is effective in increasing muscle glycogen stores after exercise. In the hours soon after exercise, consuming high–glycemic index (GI) foods can speed muscle glycogen restoration. Interestingly, Cramer et al.110 showed that fast foods (in 2 meals, including 1 meal with french fries) were similar to sports supplements of similar carbohydrate and energy content in promoting muscle glycogen resynthesis in the 4 hours following 90 minutes of glycogen-depleting cycling exercise. If a 2-hour bout of exercise reduces muscle glycogen content by 75 mmol/kg wet weight and an athlete has 6 hours of rest prior to the next exercise session, ingesting 1.0–1.2 g carbohydrate/kg BW/hour in meals or snacks could theoretically restore 60 mmol/kg wet weight, or 80% of the oxidized glycogen.
T increased levels of PS and reduced phosphatidylinositol and sphingomyelin whereas these effects were reversed by pulsed GH administration. Accordingly, co-administration of T and GH increased both hepatic and circulating TG levels to a greater extent than either hormone alone. Pulsed GH administration to TXOX induced several genes linked to unsaturated FAs biosynthesis (e.g., Fasd1, Elvol5, Fabp5), which might also contribute to lipid composition in GH- or TPGH-treated TXOX rat. Moreover, T upregulated lipogenic genes (i.e., Srebp1, Fads1, Faah), while decreased Fabp7 and FA receptor (Far4) expression, supported the lipogenic effect of T in liver. These findings agree with the observation that T increased Scd-1 gene expression, an enzyme that catalyzes the synthesis of MUFAs, mainly oleate and palmitoleate, two major components of membrane phospholipids, TG, cholesteryl esters and wax esters (86). Despite an apparent role of T, the functional role of gonadal hormones on DHA and arachidonic acid levels in hypothyroid rat liver was relevant because they were higher and lower in non-castrated hypothyroid rats than in castrated-hypothyroid rats, respectively. The levels of arachidonic acid and DHA in INTACT and TXOX rats were three-to-four times higher in total lipids than in neutral lipids (data not shown), indicating their preferential location within membrane phospholipids.
While TRT might help some people with NAFLD, it could also lead to liver enzyme changes or even worsen liver health in others. Doctors also look at other risk factors when checking the liver. If enzyme levels stay high or keep rising, more testing is usually needed to find the cause. Often, the only clue is a mild rise in liver enzymes like ALT or AST on a blood test. These tests can also help check if the liver is stiff or scarred. Doctors might need to order an ultrasound, a FibroScan, or other imaging tests to see how much fat is in the liver. A simple blood test may not be enough to tell if the liver is healthy.
With the right type of testosterone and careful monitoring, many people can take this treatment without harming their liver. Understanding how testosterone therapy affects liver enzymes helps both doctors and patients make safe choices. Regular blood tests are a good way to keep an eye on enzyme levels and make sure the liver is handling the therapy well. As testosterone levels rise, the liver has to work harder to manage the extra hormone. Testosterone therapy has grown more common, especially for men with low testosterone levels. This means that while high AST levels may suggest liver issues, they can also rise due to other problems like heart or muscle injury.
It is noteworthy that the risk for NAFLD in women with PCOS is independent of obesity or insulin resistance but is triggered directly by the hepatotoxic, destructive effect in the liver, indicated by elevated level of alanine aminotransferase . NAFLD is frequently present in PCOS women with excessive production of androgens by the ovaries and thus elevated circulating level of androgens, suggesting that abnormally high level of androgens in women may contribute to increased fat storage in the liver. The AR knockout animals are well developed, but the membrane-only AR knockout animals are not established yet, and that is why the exact role of membrane AR in liver metabolism is unclear.
When a blood test shows that liver enzymes are high, it may be a sign that the liver is under stress or damaged. These enzymes help the liver do important jobs like breaking down food, cleaning the blood, and making energy. Regular blood tests, along with good communication between the patient and doctor, are key to safe and effective hormone therapy. It also gives peace of mind to patients, knowing that their treatment is being carefully checked.

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