Key result
High-fructose or high-fat diets substantially increase adipose mitochondrial respiration in rodent models.
Why the study?
The mechanisms underlying mitochondrial respiration and morphological changes in different adipose tissues under high-fat diet and metabolic stress conditions were not fully understood.
Does not inform clinical care; leaves open whether diet-driven adipose mitochondrial changes translate to human cardiometabolic disease.
In a 24-week-long experiment, 31 rats were assigned to one of 3 groups: a Control group receiving standard chow and water, a Fructose group receiving standard chow and a 20% fructose solution, or an STZ+lipids group that received a fat-enriched diet following a single 25 mg/kg streptozotocin injection at the onset of the diet. Both groups experienced significantly increased caloric intake but did not gain weight above the Control group level. Adipocytes in subcutaneous and visceral adipose depots of both groups had smaller size compared to control and higher density in tissue. Respirometric analyses unveiled a substantial increase in mitochondrial respiration across all adipose tissue types in both dietary intervention groups, with greater changes observed in the Fructose group. Correlation analyses demonstrated that in both experimental groups high tissue respiration is associated with better biochemical profile and closer to control adipose tissue morphology. Increased tissue respiration in adipose depots could be an important mechanism of resilience to excessive caloric intake.
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Akhmetshina et al. (2023) studied this question. Fructose solution or fat-enriched diet with streptozotocin vs. Standard chow and water was evaluated on Mitochondrial respiration and morphological alterations in adipose tissues. A 20% fructose solution or a fat-enriched diet with streptozotocin substantially increased mitochondrial respiration across all adipose tissue types in 31 rats over 24 weeks.
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