Prediabetes is commonly regarded as a transitional state preceding type 2 diabetes mellitus (T2DM). However, this view does not account for its biological heterogeneity or the possibility that complications may arise before diabetes is established [1]. Skeletal fragility may be among these early manifestations. In this issue of the Korean Journal of Internal Medicine, Choi et al. [2] demonstrated that bone microarchitecture differs across prediabetic phenotypes and that these differences are, at least in part, explained by visceral adiposity.

The paradox of diabetes-related bone disease is well established. Patients with T2DM sustain more fractures despite having preserved or even increased bone mineral density (BMD) [3,4], suggesting impaired bone quality rather than reduced bone mass [3,5]. The present study extends this concept to prediabetes, indicating that alterations in bone microarchitecture may already be present at this stage. However, these changes do not appear to be uniform.

By classifying prediabetes into impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and combined IFG+IGT using oral glucose tolerance testing, the authors distinguished underlying metabolic phenotypes rather than relying on a single glycemic definition. Phenotypes characterized by postprandial dysregulation, particularly IGT, were associated with lower trabecular bone score (TBS), whereas isolated IFG was less strongly associated.

This distinction is clinically relevant. IFG and IGT are often considered together; however, they reflect different metabolic states. IFG is primarily associated with hepatic insulin resistance, whereas IGT reflects peripheral insulin resistance and postprandial glycemic excursions [6]. The present data suggest that postprandial dysregulation, rather than fasting hyperglycemia alone, may be more closely associated with alterations in bone microarchitecture.

A notable finding was the association between visceral adiposity and bone microarchitecture. Visceral fat showed the strongest association with TBS and accounted for a substantial proportion of phenotype-related differences in men with IGT. In contrast, conventional indices of insulin resistance were only weakly associated.

These findings suggest that insulin resistance may not be the principal metabolic determinant of skeletal fragility in dysglycemia. Instead, they highlight the importance of body composition, particularly visceral adiposity. This association is biologically plausible. Visceral adipose tissue functions as an active endocrine organ, producing pro-inflammatory cytokines and adipokines that influence bone remodeling by promoting osteoclast activity and inhibiting osteoblast function [7]. In addition, the coexistence of visceral adiposity and postprandial hyperglycemia may contribute to oxidative stress and the accumulation of advanced glycation end products [8], potentially compromising bone structural integrity [9].

An important observation was the lack of a consistent association between visceral adiposity and BMD. Despite the strong relationship between visceral fat and TBS, no consistent negative association was observed with BMD. These findings highlight the limitations of BMD as a surrogate marker of skeletal strength in metabolic disease [10]. Reliance on BMD alone may underestimate fracture risk in individuals with dysglycemia, particularly in those with adverse metabolic phenotypes.

Sex differences were also observed. The mediating effect of visceral adiposity was more pronounced in men than in postmenopausal women. This may reflect differences in fat distribution, with greater visceral fat accumulation in men. However, this interpretation is limited. The absence of a statistically significant total effect in women suggests that additional mechanisms, including hormonal influences and differences in adipose tissue biology, may contribute. However, these observations warrant further investigation.

Some limitations should be noted. The cross-sectional design precludes causal inference, and temporality cannot be established. Visceral adiposity and bone microarchitecture were assessed simultaneously, allowing for potential bidirectional or confounded associations. Key mediators, including inflammatory cytokines, bone turnover markers, and advanced glycation end products, were not measured. In addition, the absence of fracture outcomes limits the clinical interpretation of the observed differences in TBS.

Despite these limitations, the present study has several clinical implications. Prediabetes should not be considered a uniform condition when assessing skeletal risk. The findings also highlight the limitations of a BMD–based approach and support the incorporation of bone quality measures, such as TBS, in selected high-risk individuals. In addition, visceral adiposity may represent a modifiable factor link between metabolic and skeletal health.

These findings suggest a different perspective. The skeletal effects of dysglycemia cannot be explained by glucose levels or insulin resistance alone but likely reflect complex interactions among glycemic patterns, adipose tissue biology, and inflammatory pathways. In this context, prediabetes represents a heterogeneous metabolic condition with distinct skeletal effects.

Future studies should determine whether these phenotype-specific differences in bone microarchitecture translate into differences in fracture risk, and whether targeting visceral adiposity can modify skeletal outcomes. At present, prediabetes should not be assumed to have uniform implications for bone health.