Does Testosterone Increase Blood Sugar?

Testosterone does not simply raise or lower blood sugar. In men with low levels, restoring testosterone to a normal range tends to improve blood sugar control. Remove testosterone entirely and blood sugar climbs. But push testosterone far above normal, as with anabolic steroid abuse, and insulin resistance worsens. The relationship also differs between sexes: in women with polycystic ovary syndrome, excess testosterone is linked to higher insulin resistance, while in men the same hormone often does the opposite. The honest picture is dose-dependent, sex-specific, and shaped by factors like body fat and genetics.

Low Testosterone and High Blood Sugar in Men

The most consistent finding across decades of research is that men with low testosterone are more likely to have trouble with blood sugar. In men with type 2 diabetes, roughly 43% have reduced total testosterone, and 57% have reduced free testosterone. That association holds even in men with type 1 diabetes, and serial measurements show that as testosterone drops, insulin resistance rises.¹ Across broader populations, up to half of men with type 2 diabetes meet the criteria for hypogonadism, and their low testosterone is also tied to higher rates of cardiovascular death and all-cause mortality.²

The connection between low testosterone and poor metabolic health is not just a statistical association observed from the outside. The relationship appears bidirectional: low testosterone promotes fat gain and insulin resistance, while obesity and insulin resistance themselves drive testosterone levels down further. Inflammatory molecules and hormonal signals from excess fat tissue suppress the brain’s signaling to the testes, creating a self-reinforcing cycle.²

What Happens When You Remove Testosterone Entirely

The strongest evidence that testosterone helps regulate blood sugar comes from studies of men whose testosterone is deliberately suppressed. Men treated for prostate cancer often receive androgen deprivation therapy, which drives testosterone to near-zero levels. A meta-analysis of eight studies covering more than 150,000 men found that those on androgen deprivation had a 39% higher rate of developing diabetes compared to those not on the therapy.³ A separate study of men with localized prostate cancer found that those starting androgen deprivation had a 1.61-fold increased risk of diabetes, with about one in every 29 treated men developing the disease as a direct consequence of the therapy.⁴

The damage is not limited to new diabetes diagnoses. Among men who already had diabetes before starting androgen deprivation, blood sugar control worsened measurably. Their HbA1c, a marker of average blood sugar over a few months, rose even as doctors added more diabetes medications to try to compensate.⁵ The effect strengthened the longer men stayed on the treatment, consistent with the idea that testosterone’s metabolic benefits are ongoing rather than a one-time event.³

Does Testosterone Replacement Improve Blood Sugar?

If low testosterone is associated with high blood sugar, you would expect that restoring it helps. The evidence mostly supports this, though it is not as clean-cut as you might hope. A meta-analysis pooling 13 studies of hypogonadal men with type 2 diabetes found that testosterone therapy reduced HbA1c by a meaningful amount. In the treatment groups, HbA1c dropped from an average of about 7.2% before treatment to about 6.6% afterward, while the placebo groups stayed flat or slightly worsened.⁶ Another study showed that testosterone replacement improved fasting insulin sensitivity and reduced both HbA1c and fasting blood glucose, alongside a decrease in waist circumference.⁷

Not every trial has found this benefit, though. One well-designed randomized trial of 88 men with type 2 diabetes found that testosterone did not improve insulin resistance or HbA1c, even though it clearly changed body composition, reducing fat mass and increasing lean mass.⁸ That result is a genuine wrinkle. It suggests body composition changes do not always translate directly into better blood sugar control, and that the metabolic benefits of testosterone replacement may depend on other factors like how severely deficient someone is at baseline, whether they are on other medications, or how long treatment lasts.

When testosterone therapy does reduce inflammation, the metabolic picture tends to look more favorable. One study of men with type 2 diabetes and documented low testosterone found that treatment lowered circulating levels of C-reactive protein, tumor necrosis factor-α, interleukin-1β, and free fatty acids, all of which contribute to insulin resistance.⁹

How Testosterone Affects Blood Sugar at the Tissue Level

Testosterone influences blood sugar through several organs simultaneously, and the effects are not always in the same direction. In skeletal muscle and fat tissue, testosterone promotes the expression and activity of glucose transporters, the proteins that pull sugar out of the bloodstream and into cells. When testosterone is absent, these transporters decline and glucose uptake drops.¹⁰ Animal models of androgen deficiency confirm this: mice lacking proper androgen signaling show significantly reduced glucose transporter levels in muscle and impaired activity of the enzymes that process glucose for energy.¹¹

In the liver, testosterone plays a dual role that researchers have found genuinely surprising. On one hand, it can increase hepatic insulin resistance. On the other, it separately suppresses the liver’s tendency to pump out glucose through a pathway that operates independently of insulin signaling. In diabetic animal models, this second effect wins: even though the liver becomes slightly more resistant to insulin under testosterone’s influence, net glucose output from the liver goes down, and overall blood sugar improves.¹² When testosterone is removed by castration in animal studies, the liver ramps up glucose production and the muscles take up less, a double hit to blood sugar.¹³

There is also a more direct effect on the pancreas itself. The androgen receptor is present on the insulin-producing beta cells, and testosterone enhances their ability to secrete insulin in response to rising blood sugar. In male mice engineered to lack androgen receptors specifically on beta cells, glucose-stimulated insulin secretion drops and glucose tolerance worsens. The effect appears to work in part by amplifying the incretin system, the same pathway targeted by popular diabetes and weight-loss drugs.¹⁴

Supraphysiological Doses and Anabolic Steroid Abuse

Everything changes when testosterone climbs far above normal. Powerlifters taking large doses of anabolic steroids showed diminished glucose tolerance compared to non-users, despite producing much higher levels of insulin after a glucose challenge. Their bodies were pumping out extra insulin but it was not working properly, a hallmark of insulin resistance.¹⁵ The insulin responses in steroid users were elevated even compared to sedentary obese men, a group already prone to insulin resistance. This flips the relationship seen at low-to-normal testosterone levels: too much testosterone harms blood sugar regulation, while too little does the same. The dose-response curve for testosterone’s metabolic effects appears to be U-shaped, with a physiologically normal range as the sweet spot.

Testosterone and Blood Sugar in Women

The relationship between testosterone and blood sugar is different in women. Polycystic ovary syndrome, one of the most common hormonal conditions in women of reproductive age, is characterized by elevated testosterone and is strongly associated with insulin resistance. In a study of women with PCOS, total testosterone correlated significantly with insulin resistance scores, and elevated androgen levels were an independent predictor of insulin resistance alongside body mass and family history of diabetes.¹⁶

This sex difference is a real puzzle. In men, low testosterone predicts insulin resistance. In women with PCOS, high testosterone predicts it. The most likely explanation is that the two scenarios involve different biological contexts. In PCOS, elevated androgens are part of a broader hormonal disruption that includes altered ovarian function, abnormal signaling from fat tissue, and often elevated insulin itself, which can in turn drive the ovaries to produce more testosterone. It is less that testosterone directly raises blood sugar in women and more that testosterone excess in PCOS is a marker and participant in a wider metabolic disturbance.

Gender-Affirming Testosterone Therapy

Transgender men receiving testosterone provide a useful window into what happens when you give physiological male-range testosterone to people with a female biological baseline. A systematic review found that testosterone therapy in transgender men increased lean mass, decreased fat mass, and had no negative impact on insulin resistance.¹⁷ A separate review concluded that long-term androgen treatment brought transgender men roughly in line with cisgender men in terms of lipid profile, insulin resistance, and overall mortality, and that insulin resistance actually decreased with virilization.¹⁸

This outcome supports the idea that testosterone in the normal male physiological range does not inherently worsen blood sugar control. It also underscores the difference between the PCOS situation, where testosterone excess operates within a disrupted female hormonal environment, and gender-affirming care, where testosterone is dosed to achieve a standard male range and the underlying hormonal milieu shifts accordingly.

High Blood Sugar Also Lowers Testosterone

The relationship runs both ways. Not only does low testosterone promote insulin resistance, but high blood sugar itself damages the cells that produce testosterone. Laboratory research shows that exposing Leydig cells, the testicular cells responsible for making testosterone, to high-glucose conditions reduces their viability and their testosterone output. The cells under glucose stress show increased signs of damage and programmed cell death.¹⁹

This bidirectional relationship creates a vicious cycle in practice. A man develops insulin resistance, his blood sugar rises, the elevated glucose impairs his Leydig cells, testosterone falls, the lower testosterone worsens his insulin resistance further, and blood sugar climbs higher still. Breaking this cycle is part of the rationale for considering testosterone replacement in hypogonadal men with type 2 diabetes, even when the primary problem is metabolic rather than reproductive.

Genetic Variation in How Testosterone Affects Blood Sugar

Not every man’s body responds to testosterone the same way when it comes to blood sugar, and part of the reason is genetic. The androgen receptor gene contains a stretch of repeated DNA sequence whose length varies between individuals. The length of this repeat modifies how strongly testosterone influences insulin sensitivity. In one study, men with a repeat length at the population average saw almost no effect of changing testosterone levels on their insulin resistance. But men with longer repeats experienced a benefit: as their testosterone rose, their insulin sensitivity improved, and the longer the repeat, the bigger the improvement. Men with shorter-than-average repeats saw the opposite pattern, where rising testosterone actually worsened their insulin sensitivity slightly.²⁰

This finding helps explain why clinical trials of testosterone replacement sometimes produce mixed results. A room full of hypogonadal men with type 2 diabetes is not a genetically uniform group. Some will be strongly responsive to testosterone’s metabolic benefits and others will not, depending partly on the genetic hardware they inherited for the androgen receptor. It also suggests that the testosterone-blood-sugar connection is genuinely more complicated than a single hormone turning a single dial.

Acute Versus Long-Term Effects

The timing of testosterone’s metabolic effects adds another layer. In a crossover study of healthy men whose testosterone was temporarily suppressed and then acutely restored, short-term testosterone depletion was associated with increased oxidative glucose disposal, while a single dose of testosterone suppressed adiponectin, a protein that normally enhances insulin sensitivity.²¹ In other words, the very short-term and long-term metabolic effects of testosterone point in different directions. A quick spike in testosterone may transiently worsen certain metabolic markers, while sustained restoration improves the overall metabolic picture over weeks and months.

Animal research echoes this. In fed, resting rats, elevated testosterone promoted glycogen storage in muscles, essentially pushing glucose out of the blood and into tissue reserves. But during prolonged exercise, high testosterone could not prevent glycogen depletion and was associated with a slight dip in blood glucose.²² The practical takeaway is that testosterone’s effect on blood sugar depends not just on dose and baseline levels, but also on whether the body is at rest, exercising, fasting, or in a fed state.

What Testosterone Is Doing Through Fat Tissue

A significant portion of testosterone’s blood sugar benefit appears to work through body composition rather than through a direct switch on glucose metabolism. Testosterone reduces visceral fat, the deep abdominal fat most strongly linked to insulin resistance. In hypogonadal men with type 2 diabetes, testosterone replacement reduced waist circumference and improved the waist-to-hip ratio alongside improvements in fasting glucose and insulin sensitivity.⁷ A narrative review of the mechanisms involved identified decreases in free fatty acids and inflammatory molecules alongside increases in lean mass as key mediators: testosterone reshapes the body’s composition, and the new composition is metabolically friendlier.²³

This explains why the single trial that found no blood sugar improvement despite body composition changes is so interesting. If the fat loss and muscle gain from testosterone are supposed to be the mechanism, why did that trial not see better glucose numbers? One possibility is that the trial was shorter or the participants were on medications that masked the downstream metabolic effects. Another is that body composition is a necessary but not sufficient condition: the cellular-level changes in glucose transporters, hepatic glucose output, and beta cell function described earlier may need to be happening in concert with the body composition shift for the full benefit to appear. In men whose cellular machinery is not responding as strongly, perhaps due to genetic differences in the androgen receptor, the fat loss alone may not be enough.

Testosterone in the Context of Liver Metabolism

The liver’s response to testosterone deserves a closer look because it operates differently from muscle and fat. In normal conditions, testosterone increases insulin receptor expression in the liver and promotes glycogen synthesis, which is the liver’s way of storing glucose for later use. It also decreases the liver’s own glucose uptake and reduces fat production within the organ.²⁴ This is metabolically coherent: the liver becomes better at responding to insulin’s signal, stores more glucose as glycogen, and exports less fat into the bloodstream.

When testosterone is removed, the liver starts overproducing glucose. Castrated rats show marked increases in hepatic glucose output and gluconeogenesis, the process of manufacturing new glucose from non-sugar building blocks.¹³ The dual role described earlier, where testosterone paradoxically increases hepatic insulin resistance while simultaneously suppressing glucose output through separate pathways, means the liver’s net response to testosterone is favorable for blood sugar control even when individual signaling pathways would suggest otherwise.¹² It is the kind of finding that frustrates anyone looking for a simple answer to whether testosterone raises or lowers blood sugar.