Study summary · research use only
The AMP-activated protein kinase activator, 5-aminoimidazole-4-carboxamide-1-b-D-ribonucleoside, regulates lactate production in rat Sertoli cells
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat cell study, the authors investigated the AMP-activated protein kinase (AMPK) activator AICAR (5-aminoimidazole-4-carboxamide-1-b-D-ribonucleoside) in Sertoli cells. Cultures from 20-day-old rats were used. Western blotting showed high AMPK levels in Sertoli cells, and AICAR produced a dose- and time-dependent increase in phosphorylated AMPK, indicating enzyme activation. AICAR was associated with a dose- and time-dependent increase in lactate secretion and stimulated glucose uptake dose- and time-dependently. The authors report AICAR increased glucose transporter 1 (GLUT1) and decreased glucose transporter 3 (GLUT3) mRNA, and decreased monocarboxylate transporter 1 (MCT1) while increasing MCT4 mRNA. They conclude AICAR-activated AMPK increased lactate production, at least partly through increased glucose uptake, increased GLUT1, and altered MCT1/MCT4, suggesting a role for AMPK in Sertoli cell nutritional function.
Abstract
The aim of the present study was to investigate whether the AMP-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, is present in Sertoli cells and whether its activation by 5-aminoimidazole-4-carboxamide-1-b-d-ribonucleoside (AICAR) results in the regulation of cell metabolism to ensure lactate supply for germ cell development. Sertoli cell cultures from 20-day-old rats were used. Western blot analysis for the alpha-subunit of AMPK showed that high levels of AMPK are present in Sertoli cells. Treatment of the cultures with AICAR resulted in a dose- and time-dependent increase of P-AMPK levels indicating activation of the enzyme. A possible effect of AICAR on Sertoli cell lactate production was then analyzed. A dose- and time-dependent increment in lactate secretion was observed. The participation of AMPK activation in different biochemical processes that may be implicated in the regulation of lactate production was also analyzed. AICAR stimulated glucose uptake in a dose- and time-dependent manner. Additionally, AICAR increased the glucose transporter 1 (GLUT1) and decreased the glucose transporter 3 (GLUT3) mRNA levels. As for the role of AMPK in the regulation of the monocarboxylate transporters 1 and 4 (MCT1 and MCT4), it has been observed that AICAR treatment decreased MCT1 and increased MCT4 mRNA levels. In summary, the results presented herein show that AMPK is present in Sertoli cells and that its activation by AICAR increases lactate production as a result, at least in part, of a) an increase in glucose uptake, b) an increase in GLUT1 expression, and c) a decrease in MCT1 and an increase in MCT4 levels. Altogether, these results suggest an important role of AMPK in modulating the nutritional function of Sertoli cells.
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