Short-term refractive and choroidal changes in response to glycaemic excursions: Assessing the influence of metabolic and hormonal factors

1 | I N T RO DU CT I O N
Blurred vision is a common complication in diabetes mellitus, often
linked to acute blood glucose fluctuations.1 Despite decades of clinical
recognition, the mechanisms behind glucose-induced refractive
changes remain unclear. Numerous studies have investigated this phe-
nomenon, but findings are inconsistent2,3
: some report myopic shifts
during hyperglycaemia (“sugar myopia”),1,4 others hyperopic changes
(“sweet hyperopia”5 ) or no significant effect.6
Most models explain glucose-related refractive changes by
osmotic effects of glucose and its metabolites, altering lens-refractive
index or curvature.2,3,5,6
Hormonal factors, despite their role in glucose homeostasis, have
been largely overlooked in this context. Hormones like insulin, insulin-
like growth factor 1 (IGF-1), growth hormone (GH), and cortisol influ-
ence glycaemic regulation,7 and may also modulate ocular physiology.
Animal studies show myopic shifts following insulin administration, 8
while high cortisol levels have been linked to axial elongation and
myopia in humans.9 GH deficiency in children has been associated
with hyperopia,10 and IGF-1 genetic variants with myopia.11
Choroidal thickness (CT) is increasingly recognized as a potentially
valuable biomarker of posterior segment health. The choroid is a
highly vascularized tissue between the retina and sclera, playing a
crucial role in nutrient delivery, thermoregulation and ocular
homeostasis.12 We have previously shown that CT in the fasting state
differs significantly in individuals with obesity or type 2 diabetes
(T2D) compared with metabolically healthy controls.13 However, the
impact of acute glycaemic fluctuations on CT, particularly in diabetes,
remains poorly understood.
Here, we assessed, (i) acute glucose administration on refraction,
(ii) differences among individuals with obesity, or T2D compared with
healthy individuals, (iii) the role of insulin, cortisol, GH and IGF-1 as
potential modulators, (iv) glucose-driven changes of the CT in partici-
pants with and without obesity or T2D.