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GF Gonzales, A Cordova, K Vega, A Chung, A Villena, and C Gonez

Lepidium meyenii (Maca) is a Peruvian hypocotyl that grows exclusively between 4000 and 4500 m in the central Andes. Maca is traditionally employed in the Andean region for its supposed aphrodisiac and/or fertility-enhancing properties. This study was a 12-week double-blind, placebo-controlled, randomized, parallel trial in which active treatment with different doses of Maca Gelatinizada was compared with a placebo. The study aimed to test the hypothesis that Maca has no effect on serum reproductive hormone levels in apparently healthy men when administered in doses used for aphrodisiac and/or fertility-enhancing properties. Men aged between 21 and 56 Years received 1500 mg or 3000 mg Maca. Serum levels of luteinizing hormone, follicle-stimulating hormone, prolactin, 17-alpha hydroxyprogesterone, testosterone and 17-beta estradiol were measured before and at 2, 4, 8 and 12 weeks of treatment with placebo or Maca (1.5 g or 3.0 g per day). Data showed that compared with placebo Maca had no effect on any of the hormones studied nor did the hormones show any changes over time. Multiple regression analysis showed that serum testosterone levels were not affected by treatment with Maca at any of the times studied (P, not significant). In conclusion, treatment with Maca does not affect serum reproductive hormone levels.

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GF Gonzales, M Gasco, A Cordova, A Chung, J Rubio, and L Villegas

Lepidium meyenii (Maca) is a Peruvian hypocotyl that grows exclusively between 4000 and 4500 m in the central Andes. Maca is traditionally employed in the Andean region for its supposed fertility-enhancing properties.The aim of this study was to test the hypothesis that Maca can prevent high altitude-induced testicular disturbances. Adult male rats were exposed for 21 days to an altitude of 4340 m and treated with vehicle or aqueous extract of Maca (666.6 mg/day). The lengths of the stages of the seminiferous epithelium and epididymal sperm counts were obtained at 0, 7, 14 and 21 days of exposure. The stages of the seminiferous tubules were assessed by transillumination. A dose-response study was also performed at sea level to determine the effect of Maca given to male rats at doses of 0, 6.6, 66.6 and 666.6 mg/day for 7 days on body weight, seminiferous tubule stages and epididymal sperm count. The length of stage VIII and the epididymal sperm count were increased in a dose-dependent manner in Maca-treated rats but treatment reduced the length of stage I. At the highest dose, sperm count increased 1.58 times, the length of stage VIII increased 2.4 times and the length of stage I was reduced 0.48 times compared with the value at dose 0. Exposure to high altitude resulted in a reduction in epididymal sperm count after 7 days and lower values were maintained up to 21 days. Altitude reduced spermiation (stage VIII) to half and the onset of spermatogenesis (stages IX-XI) to a quarter on days 7 and 14 but treatment with Maca (666.6 mg/day) prevented these changes. Data on transillumination and epididymal sperm count in the Maca-treated group exposed to high altitude were similar to those obtained at sea level. Maca increased the sperm count on day 21 of exposure to high altitude to values similar (1095.25 +/- 20.41x10(6) sperm, means +/- S.E.M.) to those obtained in the Maca-treated group at sea level (1132.30 +/- 172.95x10(6) sperm). Furthermore, in the Maca-treated group exposed for 21 days to high altitude, epididymal sperm count was higher than in the non-treated group at sea level (690.49 +/- 43.67x10(6) sperm). In conclusion, treatment of rats with Maca at high altitude prevented high altitude-induced spermatogenic disruption.

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Hyun-Jeung Choi, Tae Yong Kim, Namhyun Chung, Ji Hye Yim, Won Gu Kim, Jin A Kim, Won Bae Kim, and Young Kee Shong

5-Aminoimidazole-4-carboxamide-ribonucleoside (AICAR) is an activator of 5′-AMP-activated protein kinase (AMPK), which plays a role in the maintenance of cellular energy homeostasis. Activated AMPK inhibits the protein kinase mechanistic target of rapamycin, thereby reducing the extent of protein translation and suppressing both cell growth and cell cycle entry. Recent reports indicate that AMPK-mediated growth inhibition is achieved via an action of the RAF–MEK–ERK mitogen-activated protein kinase pathway in melanoma cells harboring the V600E mutant form of the BRAF oncogene. In this study, we investigated the anti-cancer efficacy of AICAR by measuring its effects on proliferation, apoptosis, and cell cycle progression of BRAF wild-type and V600E-mutant thyroid cancer cell lines. We also explored the mechanism underlying these effects. AICAR inhibited the proliferation of BRAF V600E-mutant thyroid cancer cell lines more strongly than was the case with wild-type cell lines. The suppressive effect of AICAR on cell proliferation was associated with increased S-phase cell cycle arrest and apoptosis. Interestingly, AICAR suppressed phosphorylation of ERK and p70S6K in BRAF V600E-mutant thyroid cancer cells, but rather increased phosphorylation in wild-type cells. Together, the results indicate that AICAR-induced AMPK activation in BRAF V600E-mutant thyroid cancer cell lines resulted in increases in apoptosis and S-phase arrest via downregulation of ERK and p70S6K activity. Thus, regulation of AMPK activity may be potentially useful as a therapy for thyroid cancer if the cancer harbors a BRAF V600E mutation.

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Anna G Holmes, Jose L Mesa, Bronwyn A Neill, Jason Chung, Andrew L Carey, Gregory R Steinberg, Bruce E Kemp, Robert J Southgate, Graeme I Lancaster, Clinton R Bruce, Matthew J Watt, and Mark A Febbraio

Chronic elevations in interleukin (IL)-6 have been associated with insulin resistance, but acute IL-6 administration can enhance insulin sensitivity. Our aim was to exogenously administer IL-6 to rats to elicit either chronic or repeated acute elevations in systemic IL-6. We hypothesized that a continuous elevation of IL-6 would inhibit glucose tolerance and insulin sensitivity while acute intermittent elevations would improve it. Male Wistar rats were treated for 14d with recombinant human IL-6 (2.4 μg/day) or saline administered either by miniosmotic pump (continuous IL-6) or via twice-daily injection (intermittent IL-6). Glucose and insulin tolerance tests were performed following 14-d treatment and 24 h later rats were administered a bolus of insulin (150 mU/g) or saline intraperitoneally. Approximately, 10 min after insulin injection soleus, gastrocnemius and liver were excised and rapidly frozen in liquid nitrogen for subsequent metabolic measures. Irrespective of the mode of delivery, IL-6 treatment increased basal insulin sensitivity, as measured by the homeostatic model assessment of insulin resistance, and enhanced glucose clearance during an i.p. glucose tolerance test. IL-6 increased circulating fatty acids, but did not increase triglyceride accumulation in either skeletal muscle or liver, while it increased the protein expression of both PPARα and UCP2 in skeletal muscle, suggesting that IL-6 can enhance fat oxidation via mitochondrial uncoupling. These data demonstrate that, irrespective of the mode of delivery, IL-6 administration over 2 weeks enhances glucose tolerance. Our results do not support the notion that prolonged chronically elevated IL-6 impairs insulin action in vivo.