NEWS.

In a TriNetX target-trial emulation of post-bariatric-surgery patients, GLP-1 starters had about two fewer kidney cancers per thousand over five years than users of four other diabetes drugs. Real, consistent, and very small.

Insulin-degrading enzyme turns out to cut GLP-1 at two sites, and a mirror-image tweak to semaglutide resisted it and lasted longer in mice, including in the central nervous system.

In Florida health records, adults who regained weight after bariatric surgery took back off about half of it on a GLP-1 drug, roughly twice the non-user figure, with no rise in side effects over a year.

A drug-target Mendelian randomization study found the GIP receptor pathway, not the GLP-1 one, lined up with the broadest slower-aging profile, and blood-sugar lowering carried more of it than weight loss.

Acute kidney injury has no drug. A small peptide copied from Klotho protected mouse kidneys through both chemotherapy and blocked-blood-flow injury by guarding one mitochondrial protein, ATAD3A, from destruction and keeping the cell-death signal contained.

JP1, a peptide engineered to cross into the brain and home to motor neurons, eased paralysis and extended survival in SOD1 ALS mice by switching on the Nrf2 antioxidant and autophagy program. A clean knockout control pins the benefit to that one pathway, but the SOD1 mouse has a long record of wins that never reached patients.

A Japanese study found a third of GLP-1 users had inadequate bowel prep versus one in six non-users, and a 123,858-patient meta-analysis backs the direction. The weekly-versus-daily wrinkle and the right washout window are still guesswork.

MOTS-c is better known as an exercise-mimicking longevity signal. Glued into a gel and loaded with isolated mitochondria, it kept the cargo producing energy for up to 8 hours and, injected into rat hearts after a heart attack, reprogrammed macrophages and lifted pumping function from about 31 to 68 percent.

In 13,007 adults with a psychiatric diagnosis, starting semaglutide tracked with about a quarter fewer clinician-recorded cognitive signs over a year than no diabetes drug, glipizide or empagliflozin. Against sitagliptin, a pill that raises the body's own incretin hormones, the advantage vanished. Both readings of that null undercut a semaglutide-specific brain claim.

In people with atherosclerotic heart disease, helper T-cells reacted weakly to P210, a fragment of the LDL-carrying protein buried in artery plaques, and the weakness held a year later. A nanoparticle version of the peptide pulled that response back toward normal in the patients' own cells, a case for testing an atherosclerosis vaccine in people, not proof it works.

Osimertinib-resistant lung cancer cells make a 90-amino-acid protein translated from a circular RNA long dismissed as noncoding junk. It destroys a metabolic brake and keeps growth signaling on, a clean mechanism still confined to cells and mice.

A single-center chart review found colitis patients on semaglutide or liraglutide hit symptom remission far more often than matched controls. The effect is too large and too selection-prone to trust, but weight loss does not account for it.

In a US records study of nearly 38,000 matched adults with obesity, those who had bariatric surgery had about 60 percent lower cardiovascular risk than those on semaglutide. The catch is that the people who choose surgery are not the people who choose a shot.

A scoping review in the American Journal of Sports Medicine mapped the research behind six gray-market recovery peptides and found most of it comes from rats, with thin, uncontrolled human data and a documented heart-failure signal for MK-677.

A 1,226-person patient survey found that the more weight people lost on GLP-1 drugs, the more they reported sagging skin, hair loss, and facial hollowing, while preexisting inflammatory rashes improved. Both sides of the ledger rise with the same weight loss.