Sá nchez-Lozada LG, Tapia E, Jiménez A, Bautista P, Cristó bal M, Nepomuceno T, Soto V, Á vila-Casado C, Nakagawa T, Johnson RJ, Herrera-Acosta J, Franco M. Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. Am J Physiol Renal Physiol 292: F423-F429, 2007. First published August 29, 2006; doi:10.1152/ajprenal.00124.2006.-Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n ϭ 7) or by adding fructose to drinking water (10%, F10, n ϭ 7). Body weight and food and fluid intake of each rat were measured weekly during the follow-up. At baseline and at the end of wk 8, systolic blood pressure, plasma uric acid, and triglycerides were measured. At the end of week 8 glomerular hemodynamics was evaluated by micropuncture techniques. Wall thickening in outer cortical and juxtamedullary afferent arterioles was assessed by immunohistochemistry and computer image analysis. Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (CϽF10ϽF60). In addition, the F60 rats developed kidney hypertrophy, glomerular hypertension, cortical vasoconstriction, and arteriolopathy of preglomerular vessels. In conclusion, fructoseinduced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction. These changes are best observed in rats administered high doses (60% diet) of fructose. uric acid; obesity METABOLIC SYNDROME IS A PATHOPHYSIOLOGICAL entity characterized by insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and obesity (27). The risk for developing diabetes type 2, cardiovascular disease, and renal disease is increased with increasing manifestations of the various components of the syndrome within any individual.The macronutrient content of the diet has been linked to the metabolic syndrome. Recently, consumption of dietary fructose has been suggested to be one of the environmental factors contributing to the development of obesity and the accompanying abnormalities of the metabolic syndrome (7). In fact, a well-known experimental model of metabolic syndrome is induced by high consumption of fructose; this model induces hypertension, hypertriglyceridemia, hyperinsulinemia, and insulin resistance in rats (12). Fructose consumption is able to produce these effects because fructose is more lipogenic than glucose and usually causes greater elevations of triglycerides (10), which, in turn, increases intramyocellular triglyceride content in the skeletal muscle, causing...

NHA1 encodes a K + (Na + )/H + antiporter in the plasma membrane of Saccharomyces cerevisiae. We report that cells expressing the NHA1 gene contained less K + than the mutant lacking the gene when grown without K + limitation. They also grew better at low K + and showed higher affinity of transport than the nha1 strain. In agreement with the function of an electroneutral cation/H + antiporter, the effect was only observed at acidic pH. The improved growth and transport depended on the presence of Trk1p (the main K + influx system) and did not require the product of TRK2. We propose that Nha1p regulates the potassium content of the cell and, as a consequence, can affect the activity of the main K + influx system (Trk1p).

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The process of freezing cells or tissues and depositing them in liquid nitrogen at –196 °C is called cryopreservation. Sub-zero temperature is not a physiological condition for cells and water ice crystals represent the main problem since they induce cell death, principally in large cells like oocytes, which have a meiotic spindle that degenerates during this process. Significantly, cryopreservation represents an option for fertility preservation in patients who develop gonadal failure for any condition and those who want to freeze their germ cells for later use. The possibility of freezing sperm, oocytes, and embryos has been available for a long time, and in 1983 the first birth with thawed oocytes was achieved. From the mid-2000s forward, the use of egg vitrification through intracytoplasmic sperm injection has improved pregnancy rates. Births using assisted reproductive technologies (ART) have some adverse conditions and events. These risks could be associated with ART procedures or related to infertility. Cryopreservation generates changes in the epigenome of gametes and embryos, given that ART occurs when the epigenome is most vulnerable. Furthermore, cryoprotective agents induce alterations in the integrity of germ cells and embryos. Notably, cryopreservation extensively affects cell viability, generates proteomic profile changes, compromises crucial cellular functions, and alters sperm motility. This technique has been widely employed since the 1980s and there is a lack of knowledge about molecular changes. The emerging view is that molecular changes are associated with cryopreservation, affecting metabolism, cytoarchitecture, calcium homeostasis, epigenetic state, and cell survival, which compromise the fertilization in ART.

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GAS1 is a pleiotropic protein that has been investigated because of its ability to induce cell proliferation, cell arrest, and apoptosis, depending on the cellular or the physiological context in which it is expressed. At this point, we have information about the molecular mechanisms by which GAS1 induces proliferation and apoptosis; but very few studies have been focused on elucidating the mechanisms by which GAS1 induces cell arrest. With the aim of expanding our knowledge on this subject, we first focused our research on finding proteins that were preferentially expressed in cells arrested by serum deprivation. By using a proteomics approach and mass spectrometry analysis, we identified 17 proteins in the 2-DE protein profile of serum deprived NIH3T3 cells. Among them, Annexin A1 (Anxa1), Annexin A2 (Anxa2), dual specificity tyrosine-phosphorylation-regulated kinase 1B (Dyrk1B), and Eukaryotic translation initiation factor 3, F (eIf3f) were upregulated at transcriptional the level in proliferative NIH3T3 cells. Moreover, we demonstrated that Anxa1, Anxa2, and Dyrk1b are upregulated at both the transcriptional and translational levels by the overexpression of GAS1. Thus, our results suggest that the upregulation of Anxa1, Anxa2, and Dyrk1b could be related to the ability of GAS1 to induce cell arrest and maintain cell viability. Finally, we provided further evidence showing that GAS1 through Dyrk 1B leads not only to the arrest of NIH3T3 cells but also maintains cell viability.

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