Losing muscle (or lean mass) is a common side effect of weight loss in adults with obesity and may negatively affect metabolism and bone health. This is because muscle helps control blood sugar after meals and plays an important role in keeping bones strong, according to study lead researcher Melanie Haines, M.D., of Massachusetts General Hospital and Harvard Medical School in Boston, Mass.

Approximately 40% of the weight lost from taking semaglutide -- a type of weight-loss medication known as a GLP-1 -- comes from lean mass, including muscle. It is not yet known who is at highest risk for muscle loss or how it affects blood sugar levels, Haines said.

The researchers studied 40 adults with obesity for three months. Of these patients, 23 were prescribed semaglutide, while 17 followed a diet and lifestyle program for weight loss called Healthy Habits for Life (HHL). The researchers evaluated how their muscle mass changed.

Study participants who were prescribed semaglutide lost more weight than those who participated in the diet and lifestyle program, but the percent of weight loss that was lean mass was similar between the two groups.

After accounting for weight loss, the researchers found that in the semaglutide group, being older, female or eating less protein was linked to greater muscle loss. Also in this group, losing more muscle was linked to less improvement in blood sugar (HbA1c levels).

"Older adults and women may be more likely to lose muscle on semaglutide, but eating more protein may help protect against this," Haines said. "Losing too much muscle may reduce the benefits of semaglutide on blood sugar control. This means preserving muscle during weight loss with semaglutide may be important to reduce insulin resistance and prevent frailty in people with obesity."

Haines said that more studies are needed to find the best way to lose fat but keep muscle when using GLP-1 medications.

"Obesity is a significant risk factor for breast cancer, and while it is very preliminary data, our studies in mice suggest that these new anti-obesity drugs may be a way to reduce obesity-associated breast cancer risk or improve outcomes," said study author Amanda Kucinskas, B.S., a Ph.D. candidate in the labs of Drs. Erin Giles and Kanakadurga Singer at the University of Michigan in Ann Arbor, Mich.

Existing research has shown that having obesity can lead to worse breast cancer outcomes compared to those who do not have obesity, and weight loss can improve outcomes. However, there are many challenges with traditional weight loss methods.

Kucinskas and colleagues leveraged tirzepatide, one of a new class of effective anti-obesity medications that target GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic polypeptide) receptors. The researchers sought to learn whether or not tirzepatide would reduce obesity-associated breast cancer growth.

This mouse study included 16 mice. The 9-week-old C57BL/6 mice were fed a 40% high-fat diet and housed in a warm environment to induce obesity. At 32 weeks of age, the mice with obesity were randomly assigned injections of tirzepatide or a placebo every other day for 16 weeks. Tumor volumes were measured twice weekly.

The researchers found that the anti-obesity drug reduced body weight and body fat by approximately 20% in mice, similar to the amount of weight loss achieved by women on this drug. They found this was primarily due to a loss of adipose mass, with a reduction in adipose depot weights compared to controls.

The anti-obesity drug also reduced tumor volume compared to the controls. At the end of the study, the researchers found that tumor volume was significantly correlated with body weight, total adipose mass and the amount of fat stored in the liver.

"While these are very preliminary results, they suggest that this new anti-obesity drug may also have a beneficial impact on breast cancer outcomes," Kucinskas said.

Ongoing studies are underway in collaboration with Dr. Steve Hursting's lab at the University of North Carolina at Chapel Hill to separate the weight loss from the tumor-specific effects of tirzepatide.

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The researchers found that consuming aspartame, sucralose, glycyrrhizin and added sugars was significantly associated with a higher risk of early puberty, especially in children with certain genetic traits. The more of these sweeteners the teens consumed, the higher their risk of central precocious puberty.

"This study is one of the first to connect modern dietary habits -- specifically sweetener intake -- with both genetic factors and early puberty development in a large, real-world cohort," said Yang-Ching Chen, M.D., Ph.D., of Taipei Municipal Wan Fang Hospital and Taipei Medical University in Taipei, Taiwan. "It also highlights gender differences in how sweeteners affect boys and girls, adding an important layer to our understanding of individualized health risks."

A type of early puberty known as central precocious puberty is increasingly common. It can lead to emotional distress, shorter adult height, and increased risk of future metabolic and reproductive disorders.

Chen's previous research found that certain sweeteners can directly influence hormones and gut bacteria linked to early puberty. For example, one artificial sweetener called acesulfame potassium or AceK was shown to trigger the release of puberty-related hormones by activating "sweet taste" pathways in brain cells and increasing stress-related molecules. Another sweetener, glycyrrhizin -- found in licorice -- was found to change the balance of gut bacteria and reduce the activity of genes involved in triggering puberty.

"This suggests that what children eat and drink, especially products with sweeteners, may have a surprising and powerful impact on their development," Chen said.

The new findings come from the Taiwan Pubertal Longitudinal Study (TPLS), begun in 2018. The study included data from 1,407 teens. Central precocious puberty was diagnosed in 481 teens. The researchers assessed teens' sweetener intake through validated questionnaires and testing of urine samples. Genetic predisposition was quantified using polygenic risk scores derived from 19 genes related to central precocious puberty. Early puberty was diagnosed based on medical exams, hormone levels and scans.

Sucralose consumption was linked to a higher risk of central precocious puberty in boys and consumption of glycyrrhizin, sucralose and added sugars was associated with a higher risk of central precocious puberty in girls.

"The findings are directly relevant to families, pediatricians and public health authorities," Chen said. "They suggest that screening for genetic risk and moderating sweetener intake could help prevent early puberty and its long-term health consequences. This could lead to new dietary guidelines or risk assessment tools for children, supporting healthier development."