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Previous work from our laboratory (8) reported that testosterone administration increases androgen receptor protein content, decreases transcriptional markers of muscle proteolysis, and upregulates muscle translational capacity in young healthy mean during energy deficit. Fat accumulation due to obesity leads to increased oxidative stress levels in males (38). Nicotinic acid intake has been shown to reverse the decline in testosterone levels caused by testicular damage, demonstrating a positive effect on improving testicular function (31). Zinc, a widely recognized antioxidant, plays a critical role in testicular metabolism, and its deficiency may consequently affect testosterone levels (29).
As SREBPs are known to directly induce transcription of many genes needed for uptake and synthesis of cholesterol, fatty acids, triglycerides and phospholipids ; taken together, these data lead us to hypothesise that testosterone deficiency may diminish SAT metabolic function and reduce lipid storage capacity. Additionally, in the present study we demonstrate that mRNA expression of Srebf1 and Srebf2, key transcription factors and master regulators of lipogenesis , were significantly decreased in SAT of Tfm mice compared to testosterone treated animals and wild-type controls. In the present study we demonstrate that testosterone deficiency negatively alters the expression of targets of lipid metabolism primarily in liver and SAT but had little effect in VAT. We have also demonstrated in this study that the mRNA expression of Glucose-6-phosphate dehydrogenase (G6pd), the gateway enzyme in the pentose phosphate shunt pathway, is elevated in the liver of Tfm mice suggesting that glucose may also be utilised down this route during testosterone deficiency. Western blotting showed hepatic protein expression of FASN and ACACA to be increased in Tfm mice confirming gene expression findings.2 Testosterone treatment significantly reduced the protein expression of these enzymes versus placebo treated Tfm mice to similar levels as XY littermates.
Together, these data may suggest that, although testosterone administration increases energy expenditure in individuals with compromised muscle mass, it may not impact energy expenditure in eugonadal healthy men. The primary findings from this study were that despite higher oxygen-carrying capacity, there was no effect of testosterone on energy expenditures or whole-body substrate oxidation during 28 d of diet- and exercise-induced energy deficit. Associations between 24-h energy expenditure and activity level during energy balance (D) and energy deficit (E). Associations between 24-h energy expenditure and fat-free mass during energy balance (A) and energy deficit (B). During deficit, fat-free mass and activity factor were identified as the two primary variables accounting for the variance in 24-h energy expenditure in TEST and PLA (Figs. 3B, E). MRNA expression from rested/fasted muscle biopsies collected during energy balance (day 14) and energy deficit (day 42).
Many lifestyle habits can also significantly influence testosterone levels. From these research findings, it is evident that most studies have focused on the impact of a single dietary modification on testosterone deficiency, without considering multiple or overall dietary patterns. Surprisingly, a high-fat diet in parental generations can lead to the occurrence of testosterone deficiency in offspring (32). However, studies have also revealed that men adhering to a low-fat diet tend to exhibit lower testosterone levels (28). Although the dietary OBS alone did not demonstrate a statistically significant association with testosterone deficiency in males, the composite OBS showed a robust inverse correlation.
TFAM regulates nuclear DNA such as Serca2a expression in cardiomyocytes. TFAM also exists in subcellular compartments from which it can translocate to mitochondria. Recently, it has been demonstrated that PGC-1α is located within mitochondria, where it co-localizes within the D-loop of mtDNA with mitochondrial transcription factor A (TFAM) (49). The lower activity of the electron transport chain could be due to posttranslational modification, such as oxidation which most likely, underlies the increase in carbonylation we observed in IFM. Thus, it is possible that the reduced force generation we observed in the OQT animals is the result of the reduced state 3 activity found in this group. The higher membrane potential in the OQT group could be responsible for the increased calcium uptake we observed in the IFM.
We hypothesized that whole-body energy expenditure and fat oxidation would increase in men receiving testosterone compared with those receiving placebo. In addition, the effects of exogenous testosterone versus placebo on skeletal muscle transcriptional regulation of energy, carbohydrate, fat, and protein metabolism genes were also assessed. Whether increases in oxygen delivery capacity with testosterone administration alter whole-body energy expenditure and substrate oxidation, and skeletal muscle transcriptional regulation of energy metabolism during energy deficit remains unknown. Severe periods of energy deficit (e.g., % energy intake below energy expenditure) during arduous military training (1,2) and combat sports (3,4), causing weight loss, are known to suppress endogenous testosterone synthesis. Transcriptional regulation of energy and substrate metabolism was assessed using quantitative reverse transcription–polymerase chain reaction from rested/fasted muscle biopsy samples collected during balance and deficit. Whole-room indirect calorimetry and 24-h urine collections were used to measure energy expenditure and energy substrate oxidation during balance and deficit. The effects of testosterone on energy and substrate metabolism during energy deficit are unknown.
When 19-2H1-19-oxo-androstenedione (4-o) or -testosterone wasincubated with P450 19A1, no label(≤2%, limit of detection) derived from 18O2 was recovered in the formic acid product (detected as formate ester 3b) in three separate experiments with each substrate (FiguresS4 and S5, Supporting Information, onedata set shown for each). We designed and synthesized a new diazoalkane reagent(1-diazo-3-(3-pyridinyl)propane, 2) for formic acid derivatizationand analysis, in order to utilize liquid chromatography (LC)–massspectrometry (MS) for increased sensitivity. The analysis of trace formic acid isdifficult due to the presence of endogenous levels of the compoundin laboratory reagents, and (as did Akhtar et al.)12 we prepared 19-2H-labeled 19-oxo androstenedione(Figure 2, 4-o) and testosteronesubstrates (i.e., 19-CDO androgens) to improve the MS analysis, witha shift of +1 amu (Figure S1, Supporting Information). Observed metabolic adaptations in the current study were likely the result of high levels of daily aerobic exercise and reduced energy availability. Conversely, there was no numerical difference in protein oxidation in TEST from balance to deficit. Although glycogen content was not statistically different, a result that was driven by one outlier in TEST at deficit, it was numerically lower during deficit compared with balance.
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