GLP-1s and Testosterone: What Eight Human Studies Found

On 23 July 2026, the journal Cells published a systematic review that asked a question the literature had only answered in scattered pieces: when a man's testosterone is low and his metabolism is the reason, does treating the metabolism bring the testosterone back?

The authors registered their protocol in advance (PROSPERO CRD420261370402) and pulled together eight human studies covering roughly 1,200 men. Their answer, in men whose low testosterone travels with obesity or type 2 diabetes: total testosterone tends to rise on a GLP-1 receptor agonist, the pituitary signals that drive the testicles tend to rise with it, and sperm quality holds or improves. In healthy men without metabolic disease, the same review found no significant changes in reproductive hormones.

That boundary is most of the story. This is not a hormone drug. It is a metabolic drug whose hormonal effects show up only where metabolism was the problem.

Why a waistline moves a hormone

Functional hypogonadism, sometimes called metabolic hypogonadism, describes testicles that are structurally fine but under-instructed. The signal from the brain is turned down rather than the factory being broken.

Excess fat tissue and insulin resistance both interfere with that signal. Fat tissue converts testosterone into estradiol, which feeds back on the hypothalamus and pituitary and quiets the release of LH and FSH, the two hormones that tell the testes to make testosterone and sperm. Insulin resistance and chronic inflammation push in the same direction and drag SHBG down with them. The result on a lab report is low total testosterone with low or inappropriately normal LH and FSH: not a testicular failure, a suppressed instruction.

The Cells review frames the GLP-1 finding in exactly these terms. Where gonadotropins climbed, the authors described it as reactivation of the hypothalamic-pituitary-gonadal axis, and where SHBG climbed, as metabolic normalization. The hormone change is downstream of the metabolic change.

What the individual studies tested

Three of the studies do most of the work, and each compared a GLP-1 head to head against testosterone therapy.

Tirzepatide, 83 men, two months

A controlled pilot study in Reproductive Biology and Endocrinology enrolled 83 men with moderate to severe obesity, low testosterone, low or normal gonadotropins and insulin resistance, and split them into a tirzepatide group, a lifestyle-only group, and a transdermal testosterone group. After two months, the tirzepatide group had significantly higher LH, FSH, SHBG, and total, free and bioavailable testosterone than either comparison group, along with greater reductions in weight, waist circumference and fat mass and a larger gain in erectile function score.

The direction of the gonadotropins is the tell. In the tirzepatide group LH and FSH rose. In the transdermal testosterone group they fell by roughly a quarter, which is what exogenous testosterone does to the axis. This study was small, ran only two months, and did not randomize men to their groups, so it is preliminary.

Semaglutide, 25 men, 24 weeks

A 24-week randomized open-label trial (NCT06489457), published in Diabetes, Obesity and Metabolism and funded by the Slovenian Research Agency, compared weekly semaglutide against injectable testosterone undecanoate in 25 men with type 2 diabetes, obesity and functional hypogonadism. Both arms saw total testosterone rise, and it rose considerably more in the testosterone arm, which is unsurprising.

The divergence was in the semen analysis. In the semaglutide arm, morphologically normal sperm rose from 2% to 4% (p = 0.012). In the testosterone arm, morphology did not change while sperm concentration and total sperm number both fell significantly. With 25 men, one semen sample per timepoint and 24 weeks of follow-up, the trial's authors flagged both the sampling and the duration as limits.

Liraglutide, 110 men, four months

A prospective study in the Journal of Clinical Medicine followed 110 men aged 18 to 35 with obesity, severe erectile dysfunction unresponsive to PDE5 inhibitors, and metabolic hypogonadism. All were on a reduced-calorie diet. The liraglutide group reached significantly higher total testosterone, SHBG, LH and FSH than the groups given gonadotropins or transdermal testosterone, and its sperm motility rose from 14% to 34%. Men were assigned by whether they were currently seeking fatherhood rather than at random, and there was no placebo arm.

How confident the reviewers actually were

Not very, and they said so. Using GRADE, the review rated certainty as low for total testosterone, low to very low for free testosterone and SHBG, and very low for semen parameters. Only the metabolic outcomes, the weight and glycemic effects these drugs were built for, reached moderate certainty.

The reasons are structural rather than fixable by reading harder. The included studies were few and designed differently enough that the authors could not pool them into a meta-analysis. Follow-up was short across the board. Semen data came from very small samples and were reported inconsistently. And in most of the studies, a direct effect of the drug on the testes cannot be separated from the effect of the weight loss it produced. Nothing here measured pregnancies or live births.

What this means if you are on a GLP-1

If you are taking one of these medications for weight or diabetes and you also have symptoms of low testosterone, the useful move is measurement, not assumption. A panel that includes morning total testosterone, free testosterone, LH, FSH and SHBG distinguishes a testicular problem from a metabolic one, and repeating it after your weight has stabilized shows whether anything actually moved.

Two things are worth raising with a licensed provider. First, if fertility matters to you now or later, the contrast in these trials between what happened to sperm on a GLP-1 and what happened on testosterone therapy is a real consideration to discuss before choosing. Second, none of this evidence is strong enough to treat a GLP-1 as a hormone treatment. These are prescription medications with their own risks and side effects, and none of the studies here were designed to evaluate the safety of taking one for a hormonal reason. The hormonal effects showed up in men who already had metabolic disease, over months, in small studies. That is a reason to check your labs and to go through the risks with a licensed provider, not a reason to change your treatment on your own.

Low certainty does not mean the finding is wrong. It means the studies so far are too small and too short to tell you how large the effect is or how long it lasts.