This Week in Endocrinology — Jun 5, 2026

Welcome to This Week in Endocrinology. This week we're covering 10 notable papers spanning major shifts in disease nomenclature, new insights into diabetes risk and management, and evolving paradigms in thyroid disease. Let's dive in.

This week, a major focus is on refining our tools for both risk prediction and therapeutic development in diabetes. Kicking things off in the journal *Diabetologia*, a new trans-ancestry polygenic risk score for type 1 diabetes has been developed and validated [8]. Current risk scores, developed primarily from European data, perform poorly in other ancestries. This new score, called TA-PS, was developed using data from European, East Asian, African American, and Hispanic populations. In a multi-ancestry validation cohort, it showed significantly better predictive power than the existing European-based score, with an area under the curve of 0.89 compared to 0.85. Importantly, it provided comparable prediction across various ancestries, supporting its potential use in diverse, population-wide screening programs to identify high-risk individuals for surveillance and preventive therapies. Also in *Diabetologia*, another study offers a new tool for type 1 diabetes clinical trials [7]. Researchers analyzed data from nearly 800 participants across nine trials and found that a model-derived measure of beta cell glucose sensitivity, or βGS, served as an earlier indicator of a therapy's effectiveness compared to the traditional C-peptide area under the curve. The study suggests that baseline βGS, along with factors like age and HbA1c, could help identify individuals most likely to respond to a disease-modifying therapy, potentially streamlining future trial design. Shifting from prediction to potential treatments, a study in the journal *Diabetes* investigated LEAP2, a ghrelin receptor antagonist, in 20 men with obesity [5]. In a randomized, placebo-controlled crossover trial, a continuous intravenous infusion of LEAP2 reduced ad libitum food intake by approximately 12% and also lowered postprandial glucose excursions. These findings in humans with obesity support preclinical data and revitalize the ghrelin receptor as a potential therapeutic target for obesity and related metabolic conditions. Finally, another paper in *Diabetologia* explores the role of the gut microbiome [10]. Researchers found that indole, a tryptophan metabolite produced by gut microbes, stimulates GLP-1 secretion and promotes the differentiation of L cells in mouse models. Chronic administration of indole improved glucose tolerance and insulin sensitivity in a diabetic mouse model. These preclinical findings suggest indole acts on the gut to improve glucose homeostasis, raising the possibility of its use as a nutraceutical to help treat or prevent type 2 diabetes.

Moving from diabetes, we have two papers that redefine how we classify and understand major endocrine syndromes. First, and perhaps the biggest news of the week, comes from *The Lancet* [1]. Following a multi-step global consensus process involving over 14,000 patients and health professionals, Polycystic Ovary Syndrome, or PCOS, has been officially renamed. The new name is Polyendocrine Metabolic Ovarian Syndrome, or PMOS. The rationale is that the term PCOS is inaccurate, as it incorrectly implies pathological ovarian cysts and obscures the condition's diverse endocrine and metabolic features. The new name, PMOS, is intended to be more scientifically accurate, reduce stigma, and better reflect the condition's multisystem pathophysiology, capturing its endocrine, metabolic, and ovarian dysfunction. A global implementation strategy is now underway. In a different domain of endocrinology, a review in *The Journal of Clinical Endocrinology and Metabolism* provides an update on the genetics of familial acromegaly and pituitary gigantism [4]. While inherited forms are rare, they are clinically striking. The paper summarizes the key germline variants in genes such as AIP, MEN1, and CDKN1B, as well as X-linked acrogigantism. The authors emphasize the need for multimodal genetic testing, including next-generation sequencing and chromosome microarray, to be arranged by experienced pituitary subspecialists to fully evaluate the genetic basis of disease, which can have gene-specific therapeutic implications.

In thyroidology, we have a large-scale data analysis on the aging thyroid and a new consensus statement on nodule management. An individual participant data analysis in *The Lancet Diabetes & Endocrinology*, pooling data from over 137,000 participants across 31 cohorts, examined the natural history of thyroid function with aging [2]. Cross-sectionally, the relationship between age and TSH depended on iodine status, but longitudinal analysis showed that TSH consistently increased with age for both men and women, regardless of iodine sufficiency. The most critical clinical finding, however, was related to mortality. Compared to individuals with stable thyroid function over time, any pattern of significant change—whether TSH was increasing or decreasing—was associated with an increased risk of all-cause mortality. For example, an increasing TSH with an increasing free T4 was associated with almost two and a half times the risk of death. This suggests that while a slight TSH rise is a normal part of aging, marked instability in thyroid function is a significant risk factor. Complementing this evidence is a new joint consensus statement from the British Thyroid Association, the British Association of Endocrine and Thyroid Surgeons, and other collaborating bodies on the evaluation and management of thyroid nodules, published in *Clinical Endocrinology* [9]. While the provided abstract is a title only, this publication represents a key update to clinical guidance that practicing endocrinologists should be aware of and consult for the latest recommendations in this common clinical scenario.

Finally, we look at the role of technology and emerging environmental concerns in endocrinology. A new joint position statement from the European Association for the Study of Diabetes and the American Diabetes Association was published in *Diabetologia*, focusing on individualizing diabetes technology [6]. The statement emphasizes to healthcare professionals the importance of supporting individuals to access and use the right technology for them, based on personal needs and preferences. It makes a strong call to action to avoid disparities in providing these life-changing technologies, challenging preconceived barriers and advocating for education to minimize the 'digital divide' in diabetes care. And looking to a future challenge, a perspective piece in *The Lancet Diabetes & Endocrinology* highlights the implications of microplastics as emerging endocrine disruptors [3]. While not a primary research paper, it frames the growing concern and the urgent need for research into how chronic exposure to these ubiquitous particles may be impacting metabolic health and endocrine function.

If you only have time for one paper this week, make it the consensus statement in *The Lancet* on the renaming of PCOS to Polyendocrine Metabolic Ovarian Syndrome, or PMOS [1]. This is a fundamental change to the lexicon of our specialty for one of its most common conditions, and it will directly impact how we communicate with patients and frame management.

Here are the key takeaways from this week in Endocrinology: First: Begin preparing to use the new name for PCOS—Polyendocrine Metabolic Ovarian Syndrome, or PMOS. This reflects a global consensus to more accurately describe the condition and reduce stigma. Second: In type 1 diabetes, new tools are emerging. A trans-ancestry polygenic risk score offers more equitable risk prediction across diverse populations, while beta-cell glucose sensitivity shows promise as a more sensitive endpoint for clinical trials. Third: While TSH tends to rise with age, be aware that any significant change from an individual's baseline thyroid function, whether an increase or decrease in TSH or free T4, is associated with increased all-cause mortality. Fourth: The ghrelin receptor antagonist LEAP2 shows promise in early human studies for reducing food intake and postprandial glucose in obesity, reviving this pathway as a therapeutic target. And fifth: A new joint ADA/EASD statement calls on all of us to actively individualize diabetes technology for our patients and work to overcome the disparities that create a 'digital divide' in care.

That's your roundup for This Week in Endocrinology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

This is an automated summary generated by artificial intelligence, which can make mistakes. Always review the original source materials.