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Life sciences · Journal article
Journal of Medicine and Health Research · September 26, 2026
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Background: Adults with obesity and normal glucose regulation are widely regarded as being at low metabolic risk. Endocrine research offers a weak basis for that view because it commonly recruits participants with and without type 2 diabetes into the same cohorts. Hormonal abnormalities are therefore attributed to diabetes when they may be demonstrable well before any diagnosis. Aim: To examine hormonal control of energy expenditure and adipose tissue metabolism in adults with obesity and no diabetes diagnosis, and to relate the alterations identified to metabolic inflammation and to weight-loss resistance. Methodology: Narrative review. MEDLINE and the Cochrane Library were searched to August 2026, supplemented by Google Scholar. Priority went to systematic reviews, meta-analyses, randomised trials, prospective cohorts and mechanistic human studies in adults with overweight or obesity and no diagnosis of diabetes. No formal risk-of-bias assessment was undertaken. Findings: Clamp measurement demonstrates impaired insulin sensitivity in adults meeting every published criterion for metabolic health, so normal fasting glucose reflects beta-cell compensation rather than insulin action. Leptin is abundant and ineffective, adiponectin falls as fat mass rises, and cortisol is amplified within adipose tissue while circulating concentrations remain unremarkable. Macrophages accumulate and release cytokines that interfere with the same signalling. Energy restriction adds a second layer. Ghrelin rises, peptide YY and cholecystokinin fall, leptin and insulin fall further, and none returns to baseline within a year. Resting metabolic rate also stays suppressed below what body composition predicts, even after substantial regain. Conclusion: Weight-loss resistance in normoglycaemic obesity has a measurable biological substrate. Incretin receptor agonists achieve substantial weight loss, but weight returns on withdrawal, suggesting that they oppose these regulatory changes without resetting them. Three gaps limit what can be concluded. Definitions are not standardised, African populations are barely represented, and almost no cohort has been followed from the normoglycaemic state.