Ciencias Naturales: La Tierra por dentro: ¿estructura dinámica o estática? : Propuesta de aulas heterogéneas desde la enseñanza para la comprensión

El presente trabajo es una propuesta que fortalece la idea de que no todos aprendemos del mismo modo, así como tampoco una misma persona aprende todas las cosas con idénticos procesos. Intenta proponer un diseño de trabajo en el aula, planificado, que encierra en sí mismo una lógica de concepción sobre la enseñanza, el aprendizaje y una postura ética sobre la certeza de que todos son capaces de comprender, y además, de que esto puede materializarse a través de una enseñanza pertinente.Colegio Nacional "Rafael Hernández

Dietary and Hormonal Factors Involved in Healthy or Unhealthy Visceral Adipose Tissue Expansion

White adipose tissue (WAT) expansion is related to the development of metabolic disorders found in obesity. WAT expansion is the result of generation of new adipose cells by activation of adipogenesis and/or the increase in adipose cell size (hypertrophy). The balance between these two processes determines whether WAT expansion occurs predominantly by hyperplasia, which means the increase in the number of adipocytes, or hypertrophy. Hypertrophic adipocytes are characterized by changes in adipokine secretion pattern, insulin resistance and altered lipid metabolism, which is the reason why WAT-hypertrophic expansion is considered unhealthy. Conversely, the generation of new mature adipocytes by adipogenesis contributes to reduction of the development of hypertrophic adipocytes and therefore maintain normal WAT functions, leading to healthy hyperplastic expansion. The adipogenic capacity of adipose tissue depends on the adipogenic potential and the number of adipocyte precursor cells. Different factors are known to regulate adipogenic process and adipose tissue function, contributing to a healthy or unhealthy expansion that occurs under positive energy balance. This chapter discusses the role of fructose intake and glucocorticoids and testosterone as regulators of adipose tissue function and expansion

Effects of chronic forced circadian desynchronization on body weight and metabolism in male mice

Metabolic functions are synchronized by the circadian clock setting daily patterns of food intake, nutrient delivery, and behavioral activity. Here, we study the impact of chronic jet-lag (CJL) on metabolism, and test manipulations aimed to overcome potential alterations. We recorded weight gain in C57Bl/6 mice under chronic 6 h advances or delays of the light-dark cycle every 2 days (ChrA and ChrD, respectively). We have previously reported ChrA, but not ChrD, to induce forced desynchronization of locomotor activity rhythms in mice (Casiraghi et al. ). Body weight was rapidly increased under ChrA, with animals tripling the mean weight gain observed in controls by day 10, and doubling it by day 30 (6% vs. 2%, and 15% vs. 7%, respectively). Significant increases in retroperitoneal and epidydimal adipose tissue masses (172% and 61%, respectively), adipocytes size (28%), and circulating triglycerides (39%) were also detected. Daily patterns of food and water intake were abolished under ChrA. In contrast, ChrD had no effect on body weight. Wheel-running, housing of animals in groups, and restriction of food availability to hours of darkness prevented abnormal increase in body weight under ChrA. Our findings suggest that the observed alterations under ChrA may arise either from a direct effect of circadian disruption on metabolism, from desynchronization between feeding and metabolic rhythms, or both. Direction of shifts, timing of feeding episodes, and other reinforcing signals deeply affect the outcome of metabolic function under CJL. Such features should be taken into account in further studies of shift working schedules in humans.Instituto Multidisciplinario de Biología Celula

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

The intake of a fructose-rich diet (FRD) in the normal female rat induces features similar to those observed in the human metabolic syndrome phenotype. We studied the impact of FRD administration to mothers on pregnancy outcome. On gestational day (Gd) zero rats were assigned to either group: ad libitum drinking tap water alone (normal diet, ND) or containing fructose (10% w/vol; FRD) through pregnancy; all rats were fed a Purina chow diet ad libitum ND and FRD rats were daily cotreated or not with metformin (60 mg/Kg/day oral; ND + MF and FRD + MF) and submitted to a high glucose load test on Gd 14. Additionally, placentas from different groups were studied on Gd 20. Data indicated that: (1) although FRD rats well tolerated glucose overload, their circulating levels of insulin were significantly higher than in ND rats; (2) the mesometrial triangle blood vessel area was significantly lower in placentas from FRD than ND dams; (3) the detrimental effects of FRD administration to mothers were ameliorated by metformin cotreatment. Our study suggests that excessive intake of fructose during pregnancy enhanced the risk for developing gestational diabetes and subsequent preeclampsia, and that metformin prevented the poor pregnancy outcome induced by FRD

Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet

The intake of a fructose-rich diet (FRD) in the normal female rat induces features similar to those observed in the human metabolic syndrome phenotype. We studied the impact of FRD administration to mothers on pregnancy outcome. On gestational day (Gd) zero rats were assigned to either group: ad libitum drinking tap water alone (normal diet, ND) or containing fructose (10% w/vol; FRD) through pregnancy; all rats were fed a Purina chow diet ad libitum ND and FRD rats were daily cotreated or not with metformin (60 mg/Kg/day oral; ND + MF and FRD + MF) and submitted to a high glucose load test on Gd 14. Additionally, placentas from different groups were studied on Gd 20. Data indicated that: (1) although FRD rats well tolerated glucose overload, their circulating levels of insulin were significantly higher than in ND rats; (2) the mesometrial triangle blood vessel area was significantly lower in placentas from FRD than ND dams; (3) the detrimental effects of FRD administration to mothers were ameliorated by metformin cotreatment. Our study suggests that excessive intake of fructose during pregnancy enhanced the risk for developing gestational diabetes and subsequent preeclampsia, and that metformin prevented the poor pregnancy outcome induced by FRD.Instituto Multidisciplinario de Biología CelularCentro de Endocrinología Experimental y Aplicad

Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction

Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction

Desnaturalización de alta resolución para estudio de marcadores moleculares asociados a obesidad

El objetivo del presente trabajo fue determinar la utilidad de la técnica de “High Resolution Melting” (HRM) como método para identificar variantes en genes asociados al desarrollo de obesidad en niños

Fructose rich diet-induced high plasminogen activator inhibitor-1 (PAI-1) production in the adult female rat: Protective effect of progesterone

The effect of progesterone (P4) on fructose rich diet (FRD) intake-induced metabolic, endocrine and parametrial adipose tissue (PMAT) dysfunctions was studied in the adult female rat. Sixty day-old rats were i.m. treated with oil alone (control, CT) or containing P4 (12 mg/kg). Rats ate Purina chow-diet ad libitum throughout the entire experiment and, between 100 and 120 days of age drank ad libitum tap water alone (normal diet; CT-ND and P4-ND) or containing fructose (10% w/v; CT-FRD and P4-FRD). At age 120 days, animals were subjected to a glucose tolerance test or decapitated. Plasma concentrations of various biomarkers and PMAT gene abundance were monitored. P4-ND (vs. CT-ND) rats showed elevated circulating levels of lipids. CT-FRD rats displayed high (vs. CT-ND) plasma concentrations of lipids, leptin, adiponectin and plasminogen activator inhibitor-1 (PAI-1). Lipidemia and adiponectinemia were high (vs. P4-ND) in P4-FRD rats. Although P4 failed to prevent FRD-induced hyperleptinemia, it was fully protective on FRD-enhanced plasma PAI-1 levels. PMAT leptin and adiponectin mRNAs were high in CT-FRD and P4-FRD rats. While FRD enhanced PMAT PAI-1 mRNA abundance in CT rats, this effect was absent in P4 rats. Our study supports that a preceding P4-enriched milieu prevented the enhanced prothrombotic risk induced by FRD-elicited high PAI-1 production.Instituto Multidisciplinario de Biología CelularFacultad de Ciencias MédicasFacultad de Ciencias Exacta

Dietary and Hormonal Factors Involved in Healthy or Unhealthy Visceral Adipose Tissue Expansion

White adipose tissue (WAT) expansion is related to the development of metabolic disorders found in obesity. WAT expansion is the result of generation of new adipose cells by activation of adipogenesis and/or the increase in adipose cell size (hypertrophy). The balance between these two processes determines whether WAT expansion occurs predominantly by hyperplasia, which means the increase in the number of adipocytes, or hypertrophy. Hypertrophic adipocytes are characterized by changes in adipokine secretion pattern, insulin resistance and altered lipid metabolism, which is the reason why WAT-hypertrophic expansion is considered unhealthy. Conversely, the generation of new mature adipocytes by adipogenesis contributes to reduction of the development of hypertrophic adipocytes and therefore maintain normal WAT functions, leading to healthy hyperplastic expansion. The adipogenic capacity of adipose tissue depends on the adipogenic potential and the number of adipocyte precursor cells. Different factors are known to regulate adipogenic process and adipose tissue function, contributing to a healthy or unhealthy expansion that occurs under positive energy balance. This chapter discusses the role of fructose intake and glucocorticoids and testosterone as regulators of adipose tissue function and expansion.Facultad de Ciencias Médica

Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction

Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction.Facultad de Ciencias Médica