Jet lag is one of the most common forms of acute circadian misalignment and is experienced by millions of travellers worldwide. Experimental evidence indicates that acute circadian misalignment adversely affects metabolic regulation, including glucose metabolism (1,2). However, the extent to which these findings inform understanding of jet lag-related metabolic dysfunction remains unclear. This scoping review aimed to synthesise evidence examining the effects of acute circadian misalignment on glucose metabolism in non-shift-working healthy adults, with particular emphasis on the relevance of current evidence to jet lag and transmeridian travel. The review was conducted according to Joanna Briggs Institute methodology and reported following PRISMA-ScR guidelines. MEDLINE, Embase, PsycINFO, Web of Science and the Cochrane Library were searched from inception to 1 July 2025. Two reviewers independently screened 2,708 records and assessed 130 full-text articles, of which 21 studies met the inclusion criteria. Included studies comprised simulated night-shift protocols (n = 6), phase-shift interventions (n = 6), controlled circadian misalignment studies (n = 5), forced desynchrony protocols (n = 3), and one real-world jet lag study. Across experimental paradigms, acute circadian misalignment consistently impaired glucose metabolism, characterised by elevated postprandial glucose concentrations, impaired glucose tolerance and reduced insulin sensitivity. Reductions in insulin sensitivity were reported in 11 of 21 included studies, with directly measured impairments typically ranging from approximately 16–39% following short-term circadian misalignment. These effects occurred independently of sleep duration and energy intake and were strongly influenced by behavioural factors including meal timing and light exposure. Insulin responses were more variable, with evidence of both compensatory hyperinsulinaemia and impaired β-cell function. Night-time eating consistently worsened glycaemic control, whereas restricting food intake to daytime hours attenuated metabolic impairment. Despite strong mechanistic evidence, only one identified study directly examined glucose metabolism during transmeridian travel (3). Because laboratory models do not fully replicate the multiple behavioural and physiological disruptions associated with real-world jet lag, including altered sleep, meal timing, light exposure, physical activity and hydration, understanding of jet lag-related metabolic dysfunction remains largely dependent on laboratory-based models rather than direct observation in travellers. Given the widespread exposure of airline crew, athletes and frequent travellers to transmeridian travel, future research should prioritise ecologically valid travel studies incorporating continuous glucose monitoring and objective circadian assessment to determine the magnitude, duration and clinical relevance of jet lag-induced metabolic dysfunction and to inform practical countermeasures.