Melatonin Alleviates Liver Mitochondrial Dysfunction in Leptin-Deficient Mice.
Beatriz de Luxán-DelgadoYaiza Potes-OchoaAdrian Rubio-GonzálezJuan José SolanoJosé Antonio BogaEduardo AntuñaCristina Cachán-VegaJuan Carlos Bermejo-MilloNerea Menéndez-CotoClaudia Garcia-GonzalezGonçalo C PereiraBeatriz CaballeroAna Coto-MontesIgnacio Vega-NaredoPublished in: International journal of molecular sciences (2024)
Despite efforts to elucidate the cellular adaptations induced by obesity, cellular bioenergetics is currently considered a crucial target. New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatment on mitochondrial function and lipid metabolism in the livers of leptin-deficient mice. Our results revealed that the absence of leptin increased lipid storage in the liver and induced significant mitochondrial alterations, which were ultimately responsible for defective ATP production and reactive oxygen species overproduction. Moreover, leptin deficiency promoted mitochondrial biogenesis, fusion, and outer membrane permeabilization. Melatonin treatment reduced the bioenergetic deficit found in ob/ob mice, alleviating some mitochondrial alterations in the electron transport chain machinery, biogenesis, dynamics, respiration, ATP production, and mitochondrial outer membrane permeabilization. Given the role of melatonin in maintaining mitochondrial homeostasis, it could be used as a therapeutic agent against adipogenic steatosis.
Keyphrases
- oxidative stress
- high fat diet induced
- insulin resistance
- metabolic syndrome
- reactive oxygen species
- type diabetes
- weight loss
- diabetic rats
- high intensity
- fatty acid
- adipose tissue
- combination therapy
- replacement therapy
- high fat diet
- drug induced
- body mass index
- mouse model
- quality improvement
- high glucose
- solar cells