Submitted:
09 September 2026
Posted:
10 September 2026
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Abstract
Background: Excessive pubertal sucrose intake is a growing public health concern; however, its effects on cholesterol metabolism and male reproductive endocrinology during this developmental window remain poorly understood, particularly at concentrations within the range of habitual human consumption. The reported effects of dietary sugar on circulating testosterone levels are inconsistent. We hypothesized that the developmental stage of exposure accounts for this discrepancy. Methods: Male ICR mice were provided free access to a 10% (w/v) sucrose solution from 4 to 8 weeks of age. We assessed hepatic and plasma lipids, testicular cholesterol and testosterone concentrations, hepatic acetyl-CoA carboxylase (ACC) and AMPK phosphorylation, and the expression of cholesterol metabolism- and steroidogenesis-related genes. Results: Sucrose intake selectively elevated hepatic and plasma cholesterol levels without altering triglyceride levels, and the increase in circulating cholesterol was confined to the non-high-density lipoprotein fraction. Hepatic transcriptional changes were selective rather than uniform, with the largest increase observed for Abcg5. The phosphorylation of both ACC1 and ACC2 was elevated without any change in AMPK phosphorylation. The peritesticular fat weight increased despite unchanged body weight and energy intake. In the testes, cholesterol content and Stard3, Hsd3b1, Cyp17a1, and Hsd17b3 mRNA levels were increased, whereas steroidogenic enzyme protein levels remained unchanged. Plasma testosterone levels significantly increased, whereas intratesticular testosterone levels did not. Conclusions: Pubertal sucrose intake at a physiologically relevant concentration resulted in a cholesterol-predominant rather than triglyceride-predominant lipid response and elevated circulating testosterone levels. The increase in testicular cholesterol without a corresponding increase in steroidogenic enzymes suggests that enhanced substrate availability, rather than enzymatic capacity, may underlie this elevation.
Keywords:
sucrose
; puberty
; cholesterol
; steroidogenesis
; testosterone
; non-HDL-cholesterol
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