The study set out to answer a deceptively simple question: how do the growth hormone and insulin-like growth factor 1 pathways, often abbreviated as the GH/IGF-1 axis, behave in children whose insulin-producing cells have been destroyed by autoimmune attack? This axis is a cornerstone of pediatric physiology. The pituitary gland releases growth hormone in pulses, and the liver responds by producing IGF-1, which drives linear growth, muscle development, and cellular repair. Because insulin is a key permissive signal in this system, chronic insulin deficiency and the metabolic chaos of poorly controlled diabetes can theoretically dampen the entire axis. Testing that idea in a real pediatric population required careful measurement of hormones, growth parameters, and liver health in the same group of children.

The researchers enrolled 250 children with type 1 diabetes at a single center and performed a battery of assessments on each participant. These included standard anthropometric measurements such as height and body mass index, laboratory determination of growth hormone and IGF-1 levels measured by enzyme-linked immunosorbent assay, glycated hemoglobin, or HbA1c, as an index of average blood sugar control over the preceding months, and liver ultrasonography to screen for fatty liver disease. The team then applied multivariate logistic and linear regression models to identify which factors independently predicted MASLD and which predicted impaired linear growth. This statistical approach allowed them to disentangle the effects of age, sex, disease duration, glycemic control, and liver status from one another.

The results were sobering. The cohort’s mean HbA1c was 10.8 percent, a figure far above the recommended targets for children with diabetes and a clear indicator that, as a group, these children experienced prolonged periods of significant hyperglycemia. Against that backdrop, liver ultrasonography revealed MASLD in 36 percent of the participants, meaning roughly one in three children already carried fat deposits in the liver, a condition more commonly associated with obesity and insulin resistance than with type 1 diabetes. Equally striking was the hormonal picture: age-adjusted IGF-1 levels were reduced in 60 percent of the children, a majority of the cohort showing evidence of a blunted growth hormone axis.

When the researchers used regression analysis to identify independent predictors of MASLD, three factors emerged. Longer disease duration carried an odds ratio of 1.180, meaning each increment in the time a child had lived with diabetes increased the odds of fatty liver. HbA1c levels carried an odds ratio of 1.146, confirming that poorer glycemic control independently raised MASLD risk. Alanine aminotransferase, a liver enzyme released when hepatocytes are damaged or stressed, carried an odds ratio of 1.028, consistent with the biochemical signature of hepatic fat accumulation. Taken together, these predictors paint a coherent picture: the longer and more severely a child’s diabetes runs out of control, the more likely the liver is to accumulate fat.

Perhaps the most provocative finding concerned the relationship between fatty liver and the growth hormone axis. The presence of MASLD significantly increased the risk of reduced IGF-1 levels, with a relative risk of 1.841 and a 95 percent confidence interval of 1.113 to 3.044. Because that confidence interval excludes the value of 1, the association is statistically significant, and the magnitude suggests that children with fatty liver were nearly twice as likely to have low IGF-1 as those without it. The authors interpret this as evidence of significant hormonal dysregulation linked to insulin deficiency and metabolic decompensation. In other words, the liver, which is both the main source of circulating IGF-1 and the organ burdened by fat infiltration, may be failing on both fronts simultaneously in these children.

The story of linear growth proved more nuanced. On initial analysis, IGF-1 levels correlated with height, which would fit the textbook expectation that more growth factor means taller children. However, once the researchers adjusted for age and sex, that association lost statistical significance. What remained robust was disease duration, which stood out as a strong negative predictor of linear growth with a p-value of 0.000. This suggests that the cumulative burden of living with type 1 diabetes, rather than any single hormonal measurement, is what erodes a child’s growth trajectory over time. Chronic metabolic decompensation, recurrent insulin deficiency, and the hormonal disruptions documented in the study appear to accumulate, quietly constraining growth year after year.

Why should fatty liver disease appear in children with type 1 diabetes at all? The condition, now termed MASLD to reflect its metabolic underpinnings, is classically driven by insulin resistance, in which high circulating insulin levels push the liver to synthesize and store fat. Type 1 diabetes is defined by insulin deficiency rather than resistance, yet children with the disease are not immune to the metabolic syndrome, particularly when glycemic control is poor, body weight rises with exogenous insulin therapy, and fluctuating glucose levels create cycles of over- and under-insulinization. The high mean HbA1c in this cohort indicates that many of these children experienced exactly the kind of metabolic instability that can promote hepatic fat deposition even in the absence of endogenous insulin production.

The clinical implications are significant. First, the study suggests that liver ultrasonography and alanine aminotransferase monitoring deserve a place in routine pediatric diabetes care, since more than a third of these children had MASLD that could otherwise progress silently toward inflammation and fibrosis. Second, the high prevalence of reduced IGF-1 raises the question of whether growth monitoring and, where clinically indicated, assessment of the GH/IGF-1 axis should be integrated into follow-up for children with long-standing or poorly controlled diabetes. Third, the identification of HbA1c and disease duration as modifiable or trackable risk factors gives clinicians concrete targets: intensifying glycemic management early in the disease course may protect both the liver and the growth axis before irreversible damage accumulates.

The research, led by Feruzakhan Uvaidillaeva of the Kyrgyz-Russian Slavic University together with colleagues at the Kyrgyz State Medical Academy and the International Higher School of Medicine, was approved by the ethics committee of the Kyrgyz Medical Academy and conducted with informed consent from parents or legal guardians. As a single-center cross-sectional study, it captures a snapshot rather than a trajectory, so future longitudinal work will be needed to confirm whether fatty liver disease drives the hormonal changes, whether both are downstream of the same metabolic derangement, or whether the relationship runs in both directions. What the study establishes is that in children with type 1 diabetes, poor glycemic control and longer disease duration are the major factors associated with MASLD, and that MASLD itself travels with dysregulation of the GH/IGF-1 axis. For the millions of families managing type 1 diabetes worldwide, the message is clear: the disease’s reach extends well beyond blood sugar, into the liver and the very hormones that govern a child’s growth.

Subject of Research: GH/IGF-1 axis dysregulation and MASLD risk in children with type 1 diabetes

Article Title: Hormonal dysregulation of the GH/IGF-1 axis and its association with MASLD risk in children with type 1 diabetes

Article References: Uvaidillaeva, F., Tuhvatshin, R., Alisherova, A., Kniazeva, V., Omurkulova, B., Kim, T., & Toigonbaeva, B. (2026). Hormonal dysregulation of the GH/IGF-1 axis and its association with MASLD risk in children with type 1 diabetes. BMC Endocrine Disorders. https://doi.org/10.1186/s12902-026-02601-7

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02601-7

Keywords: type 1 diabetes, MASLD, fatty liver disease, growth hormone, IGF-1, HbA1c, pediatric endocrinology, liver ultrasonography, glycemic control, linear growth, alanine aminotransferase, metabolic decompensation