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However, testosterone concentration in this patient was among the highest reported for women with androgen-producing tumors (19,20). The progressive worsening of insulin sensitivity following tumor removal indicates that in this patient the general effect of testosterone was sensitizing. These data from a postmenopausal woman before and after surgical correction of extreme hyper-testosteronemia suggest that testosterone may affect insulin sensitivity. Interestingly, the response of hepatic glucose production to insulin was incomplete preoperatively and improved 1 month postoperatively, indicating increased liver insulin sensitivity. Conversely, ITT and glucose clamp indicated deterioration of peripheral insulin sensitivity 1 month postoperatively (decreased kITT and glucose utilization), which remained unchanged 9 months postoperatively. OGTT revealed moderate insulin resistance and glucose intolerance preoperatively that remained unchanged 1 month postoperatively; 9 months postoperatively, OGTT became diagnostic for type 2 diabetes..|The onset of the millennium was accompanied by a significant surge in both testosterone testing and initiation of testosterone replacement, especially in men without clear indications (1). By dissecting the hypothalamic-pituitary-gonadal axis, we demonstrated that the cause of low testosterone was a decrease in testicular responsiveness to luteinizing hormone (LH).|Shaded area represents values for subjects with hypogonadal testosterone levels (i.e., 2 max) (C) and expression of UQCRB in skeletal muscle (D). Correlation between insulin sensitivity (M) and serum testosterone (T) levels (A) and SHBG levels (B) in 60 men; 27 had NGT (□), 12 had IGT (△), and 21 had type 2 diabetes (•). In terms of addressing causality, it has been shown that improving insulin sensitivity by losing weight, whether by lifestyle changes or bariatric surgery, results in a significant increase in total testosterone levels (17). We and others have shown that testosterone levels are significantly lower in men with impaired glucose tolerance and T2DM than in normoglycemic controls (16). Men with hypogonadal testosterone levels were twice as insulin resistant as eugonadal controls. Given that low testosterone levels predict type 2 diabetes mellitus (T2DM) in men, we sought to dissect the relationship between testosterone and insulin sensitivity in men.|For some parameters like prostate cancer, the studies were not adequately powered and/or of sufficient duration to rule out an effect. In addition, data from our group led to the recommendation that testosterone be measured in the fasting state. Therefore, a low testosterone level must always be confirmed by repeat testing before a diagnosis of hypogonadism can be established.|Think of a hormone as a key and the cells of its target tissue, such as an organ or fat tissue, as specially shaped locks. Scientists have identified over 50 hormones in the human body so far. Hormones are chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, skin, muscles and other tissues. In some individuals, yes—but improvements are more closely tied to insulin sensitivity than weight alone.|In contrast, in females, increasing circulating testosterone concentrations to levels observed in males activates AR in β cells to enhance GSIS in a non-physiological manner, leading to mitochondrial dysfunction, oxidative stress, and ultimately resulting in β cell dysfunction that predisposes to diabetes. In males, physiological concentrations of testosterone enhance GSIS in a physiological manner, and loss of AR action in β cells produces insulin deficiency, which predisposes to diabetes. The studies reviewed here demonstrate that testosterone acts in β cells to differentially modulate β cell function in males and females. The developmental effect of testosterone alters insulin secretion in adult female offspring, leading to basal hyperinsulinemia (independent from insulin resistance) but reduced insulin secretion in response to β cell dysfunction, as observed in adult females with androgen excess. These mice remained normoglycemic in the fasting and fed states and during a glucose challenge, demonstrating that, during testosterone excess, AR activation in β cells is necessary for the development of hyperglycemia in female mice. Testosterone excess may predispose women to T2D via chronic AR activation in pancreatic islet β cells, producing insulin hypersecretion and secondary β cell failure. Since the AR is expressed in β cells in females, this raises the possibility that excess testosterone produces insulin hypersecretion and β cell dysfunction.|Therefore, the integration of androgenic and metabolic signals could be an evolutionary strategy to enhance muscle anabolism and glycogen storage in males when food is available. The evolutionary and biological basis for testosterone stimulation of insulin secretion in males is likely to promote anabolism, since both testosterone and insulin are anabolic hormones. Surprisingly, male rats with castration-induced testosterone deficiency exhibit a decrease in β cell mass due to increased apoptosis and decreased proliferation, but this is not observed in castrated male mice (Harada et al., 2018). Testosterone action on an extranuclear AR in β cell amplifies the insulinotropic action of islet-derived GLP-1 via increasing cAMP production and PKA activation. We reasoned that because GLP-1 is secreted by α-cells (Liu et al., 2011, Marchetti et al., 2012), testosterone would enhance GSIS in cultured islets but not in cultured INS-1 cells (which do not secrete GLP-1). Together, these observations suggest that testosterone is necessary for normal GSIS in men, and that men with androgen deficiency (e.g., those undergoing ADT) develop β-cell dysfunction that predisposes them to T2D. This suggests that the hyperglycemia observed in patients treated by ADT is at least partially due to β cell dysfunction leading to insulin deficiency.|Over the past decade, a number of randomized, placebo-controlled clinical trials have been conducted to determine the impact of testosterone replacement on a variety of clinically important endpoints in middle-aged and older men (12–15). Importantly, in 15% of men, testosterone levels declined into the hypogonadal range, indicating the potential to make an erroneous diagnosis of hypogonadism if testosterone is measured after eating. By contrast, men begin to experience a decline in testosterone levels in the 4th decade; given that the rate of decline is only about 2% per year, any decline remains within the normal range for many men (6). All women ultimately experience a drop in estradiol levels into the menopausal range. In addition, it is important to appreciate that while the term "andropause" was introduced to draw an analogy between age-related changes in testosterone in men and that of menopause in women, there are clear and important differences. However, as I and others pointed out, there were insufficient data from clinical trials at that time to permit any major conclusions about the role of androgen replacement in the treatment of age-related physiological changes (5). Magazine and TV advertisements encouraged men to have their testosterone levels checked if they felt in any way below par and touted the myriad benefits of testosterone replacement.}
Thus, we speculate that whether it is possible to check up-regulation in mRNA expression no modifications can be described on protein expression levels. Herein, T or I treatment increased Glut4 mRNA, but not protein expression. Principally, I activates the p21ras/MAP kinase (MAPK) (RAS)/extracellular-signal-regulated kinase (ERK) and the Phosphoinositide 3-kinase (PI3 K)/AKT pathways known to play different role in I-mediated effects. To date, 14 glucose transporters isoforms with a specific pattern of tissue expression have been identified . GLUT4 mediates glucose uptake in adipose tissues and striated muscle.
Observational studies show that long-term therapy with testosterone prevents progression from prediabetes to diabetes and improves HbA1c. Testosterone enhances insulin sensitivity in obese men with hypogonadism by decreasing fat mass, increasing lean mass, decreasing free fatty acids and suppressing inflammation. This narrative review is focused on detailing the mechanisms that underlie the metabolic aspects of testosterone therapy in humans. Effect of testosterone on I-related metabolic pathways. Effect of testosterone on Glut4 mRNA expression. T-related effects were shown to be androgen receptor dependent. Moreover, if our data are confirmed we could also state that athletes often acutely abuse with T also because of the rapid effects on T metabolic I-related pathways, in addition to possible rapid effects of T on neuromuscular system .
The normal aging process is accompanied by physiological changes in target organs that are sites of androgen action. However, the approval of a transdermal testosterone delivery system in the form of a gel meant that testosterone could now be administered easily, conveniently, and in a pain-free manner (3). For decades, the only method of delivering testosterone was through a deep, painful intramuscular injection every two weeks. A second important factor that contributed to the more widespread use of testosterone was the development of more patient-friendly formulations. While increasing awareness of and demand for a medication may be beneficial if the risk-benefit ratio of the drug is favorable, that assumption is questionable for many men taking testosterone for nonspecific symptoms without a clear diagnosis. When prescribing trends are compared between countries, it is evident that this increase in testosterone use was most marked in the United States, with relatively little change in the United Kingdom (1).
Further, in cultured mouse and human islets, testosterone also amplifies the insulinotropic effect of exogenous GLP-1. It also suggests that testosterone amplifies the insulinotropic effect of islet-derived GLP-1 in vivo. For that reason, we explored the possibility that AR action in β-cells amplifies GLP-1R signaling to increase cAMP production. Interestingly, in β-cells, AR exhibits a predominant extranuclear location and remains extranuclear following ligand stimulation. In classical androgen-sensitive tissues, AR is a ligand-activated nuclear receptor that regulates gene expression through binding to an androgen response element on the promoter of target genes (Chang et al., 1988, Lubahn et al., 1988, Tilley et al., 1989).
We have investigated the short-term effects of T on human muscle metabolic functions in vitro using human cultures of fetal skeletal muscle cells (Hfsmc) treated with T (100 nM) or insulin (I) (100 nM). Independently from cells differentiation status, testosterone, with an insulin-like effect, induced Glut4-mRNA expression, GLUT4 protein translocation to the cytoplasmic membrane, while no effect was observed on GLUT4 protein expression levels. In females, testosterone excess in β cells promotes insulin hypersecretion, mitochondrial dysfunction, oxidative stress and predisposes to β cell dysfunction and failure. In males testosterone action in β cells increases GSIS by enhancing GLP-1 insulinotropic action, prevents inflammation and promote β cell health.
Oocyte quality improvements, relevant for women undergoing IVF, are assessed after a full follicular cycle of supplementation, approximately 90 days. Insulin and testosterone markers improve earlier, typically within 6 to 8 weeks. Powder formulations generally offer better dose flexibility than capsules for women who need to adjust based on cycle response. The two forms of inositol are chemically similar enough that manufacturing quality matters — impurities or mislabeling of the ratio affects outcomes. This is also the formulation to use when estrogen is low or borderline — because high d-chiro-inositol will lower it further through aromatase inhibition. The researchers concluded that d-chiro-inositol at supraphysiological concentrations induces "inositol paradox" in the ovaries, impeding the very follicular development it is meant to support.
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