GLP-1 drugs have transformed the conversation around obesity and diabetes. Medicines such as semaglutide and liraglutide are widely known for helping people lose weight, improve blood sugar control and, in many cases, reduce the risk of metabolic complications. But researchers are now looking at another possible effect: what happens to testosterone levels in men taking these medicines? The question is particularly relevant for men with obesity, insulin resistance or type 2 diabetes, conditions that can themselves be linked to low testosterone. Emerging research suggests that GLP-1 receptor agonists may be associated with improvements in testosterone levels in some men. However, experts caution against calling these medicines “testosterone boosters”. Their possible hormonal benefits may instead be a consequence of improving the metabolic problems that can suppress testosterone production. Dr Nishant Raizada, Head, Endocrinology, Amrita Hospital, Faridabad, explains why the relationship between obesity, metabolism and testosterone is more complicated than it may appear.

How Is Obesity Linked To Low Testosterone?

Low testosterone in men with obesity is not necessarily caused by a problem with the testicles themselves. Excess body fat, particularly visceral and abdominal fat, can interfere with the hypothalamic-pituitary-gonadal (HPG) axis, the hormonal signalling system that connects the brain and reproductive organs.

Insulin resistance, chronic low-grade inflammation, changes in leptin signalling and increased conversion of testosterone into oestrogen in adipose tissue may all contribute to hormonal disruption.

This means that when an overweight or obese man has low testosterone, simply looking at testosterone production in isolation may not provide the complete picture.

“I would not call GLP-1 medicines ‘testosterone-boosting drugs'. That would be scientifically incorrect. They may lift some of the metabolic brakes on normal testosterone production,” says Dr Raizada.

What Does The Research Say About GLP-1 Drugs And Testosterone?

Research into the relationship between GLP-1 receptor agonists and male hormones is still developing, but the findings so far are interesting. A systematic review and meta-analysis published in 2025, which included seven studies and 680 participants, found that treatment with GLP-1 receptor agonists was associated with an increase in total testosterone. The treatment was also associated with reductions in body weight, BMI, waist circumference and HbA1c.

Another systematic review published in 2026 looked at 10 studies involving 639 men. It found that total testosterone generally increased during GLP-1 therapy, particularly among men with obesity, type 2 diabetes or functional hypogonadism. However, the results were less consistent when researchers looked at free testosterone. This distinction matters because total testosterone and free testosterone are not interchangeable. Most testosterone in the blood is bound to proteins, while only a small proportion circulates in an unbound or “free” form. Free testosterone is biologically available to tissues.

Therefore, an improvement in one testosterone measurement does not necessarily mean that every aspect of androgen function has changed in the same way.

Is The Testosterone Increase Directly Caused By GLP-1 Drugs?

Not necessarily. One of the biggest questions researchers are trying to answer is whether GLP-1 medicines have a direct effect on the reproductive hormone system or whether improvements in testosterone are mainly a result of weight loss and better metabolic health. Obesity can suppress normal reproductive hormone signalling. When body weight, insulin resistance and metabolic health improve, some of those hormonal disturbances may also improve.  This could explain why testosterone rises in some men after starting GLP-1 therapy.

In other words, the medicine may not be acting like testosterone replacement therapy. Instead, it may be helping address some of the underlying metabolic factors associated with low testosterone.

GLP-1 Drugs Vs Testosterone Therapy: Why The Difference Matters

One study comparing liraglutide with testosterone replacement therapy in obese men with functional hypogonadism provides an interesting insight. After 16 weeks, testosterone levels increased in both groups. However, the men receiving liraglutide experienced substantially greater weight loss, losing an average of 7.9 kg compared with about 0.9 kg in the testosterone-treatment group.

Liraglutide was also associated with increases in luteinising hormone (LH) and follicle-stimulating hormone (FSH), hormones involved in the body's natural reproductive signalling. The distinction is clinically important.

Testosterone replacement can increase testosterone circulating in the blood, but externally administered testosterone can suppress the body's own LH and FSH production. This can reduce stimulation of the testes and may affect sperm production and fertility. GLP-1 medicines work through a fundamentally different pathway.

“This is why the question should not simply be, ‘How do we raise the testosterone?' For some men, we also need to ask, ‘What is holding it back in the first place?'” says Dr Raizada.

What About Fertility And Sperm Quality?

"The relationship between GLP-1 therapy, testosterone and male fertility is another area attracting attention. A small randomised trial involving men with obesity, type 2 diabetes and functional hypogonadism compared semaglutide with testosterone therapy over 24 weeks. Researchers assessed hormonal outcomes as well as semen-related parameters. These early findings are important because testosterone levels alone do not determine male fertility. In fact, taking testosterone replacement without medical supervision can negatively affect sperm production," says Dr Raizada. 

However, the available evidence on GLP-1 drugs and fertility remains limited. Larger and longer studies are needed before these medicines can be considered a treatment for male infertility or low testosterone.

Does Weight Loss Automatically Increase Testosterone?

Not every man who loses weight will experience the same hormonal changes. The extent of improvement can depend on the underlying cause of low testosterone, the degree of obesity, insulin sensitivity, sleep quality, age, medications and other health factors.

Sleep is particularly relevant because poor sleep and conditions such as obstructive sleep apnoea can also be associated with reduced testosterone levels.

Nutrition and excessive calorie restriction may also influence reproductive hormones. Therefore, testosterone should be considered as part of a broader picture of metabolic and overall health rather than as an isolated laboratory number.

Are GLP-1 Drugs A Treatment For Low Testosterone?

The current evidence does not support using GLP-1 receptor agonists simply as testosterone-raising medicines. These drugs are primarily prescribed for conditions such as obesity and type 2 diabetes, depending on the specific medicine and indication. A man experiencing symptoms such as reduced libido, erectile difficulties, fatigue, reduced muscle mass or other symptoms associated with low testosterone should not start a GLP-1 drug or testosterone therapy without medical evaluation.

Low testosterone also needs to be properly diagnosed. Testosterone levels can fluctuate, and a single test may not be enough to establish hypogonadism. Doctors may consider repeat morning testosterone measurements along with symptoms and, when appropriate, other hormone tests to determine the underlying cause.

The emerging connection between GLP-1 drugs and testosterone is certainly interesting, but it is too early to describe these medicines as hormonal treatments. Research suggests that total testosterone may increase in some men receiving GLP-1 receptor agonists, particularly those with obesity, type 2 diabetes or functional hypogonadism. At the same time, changes in free testosterone and sex hormone-binding globulin have been less consistent.

“A meta-analysis in 2025 demonstrated significant improvement in bioavailable testosterone with GLP-1 receptor agonists, but changes in free testosterone and sex hormone-binding globulin were not statistically significant. Larger, better-powered trials are still needed,” says Dr Raizada. For now, the bigger lesson may be that testosterone cannot always be separated from metabolic health.

Obesity, insulin resistance, poor sleep and other metabolic problems can influence the hormonal environment in which testosterone is produced and regulated. Improving those factors may, in some men, allow testosterone levels to recover naturally.

So, rather than viewing GLP-1 medicines as a shortcut to higher testosterone, experts say the focus should remain on treating the underlying metabolic problem when that is the driver of hormonal dysfunction.

The important question may not simply be, “How can we increase testosterone?” It may be: “Why is testosterone low in the first place?” And that shift in perspective could prove more important than the number on a testosterone report.



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