<p>Markers of α2- and β1-adrenergic receptors (AR) were detected immunohistochemically in the liver of <i>db/db</i> mice with obesity and type 2 diabetes mellitus before and after melatonin treatment. Melatonin (1 mg/kg in 200 μl distilled water) was administered intragastrically from the 8th to the 16th week of life. The comparison groups were intact and placebo-treated <i>db/db</i> mice. Melatonin administration resulted in a significant increase in the relative areas of β1- and α2-AR expression, with a tendency towards an increase in the area ratio, as well as a significant increase in the ratio of β1/α2-AR concentrations due to preferential increase in β1-AR parameters. Melatonin administration apparently reduces sympathetic neuropathy of the liver and promotes the shift of lipid metabolism processes in hepatocytes towards lipolysis activation, which allows us to consider this hormone as a promising component of complex therapy of fatty liver disease.</p>

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Effect of Melatonin on the Expression of α2- and β1-Adrenergic Receptors in the Liver of db/db Mice. Immunohistochemical Characteristics

  • S. V. Michurina,
  • S. I. Kolesnikov,
  • D. V. Vasendin,
  • I. Yu. Ishchenko,
  • S. A. Arkhipov

摘要

Markers of α2- and β1-adrenergic receptors (AR) were detected immunohistochemically in the liver of db/db mice with obesity and type 2 diabetes mellitus before and after melatonin treatment. Melatonin (1 mg/kg in 200 μl distilled water) was administered intragastrically from the 8th to the 16th week of life. The comparison groups were intact and placebo-treated db/db mice. Melatonin administration resulted in a significant increase in the relative areas of β1- and α2-AR expression, with a tendency towards an increase in the area ratio, as well as a significant increase in the ratio of β1/α2-AR concentrations due to preferential increase in β1-AR parameters. Melatonin administration apparently reduces sympathetic neuropathy of the liver and promotes the shift of lipid metabolism processes in hepatocytes towards lipolysis activation, which allows us to consider this hormone as a promising component of complex therapy of fatty liver disease.