Expression of fibroblast growth factor-8 and its cognate receptors, fibroblast growth factor receptor (FGFR)-3c and-4, in fetal bovine preantral follicles

Paracrine cell signaling is thought to be important for ovarian follicle development, and a role for some members of the fibroblast growth factor (FGF) family have been suggested. In the present study, we tested the hypothesis that FGF-8 and its cognate receptors (FGFR-3c and FGFR-4) are expressed in bovine preantral follicles. Reverse transcription-polymerase chain reaction was used to amplify bovine FGF-8, FGFR-3c, and FGFR-4 from preantral follicle samples and a variety of fetal and adult tissues. All three genes were widely expressed in fetal tissues, with a restricted expression pattern in adult tissues. FGF-8 and FGFR-3c were expressed in secondary follicles in 70% of fetuses examined, whereas FGFR-4 expression was significantly less frequent (20%). FGFR-3c expression frequency was significantly lower in primordial compared to secondary follicles, and FGF-8 expression showed a similar trend. FGFR-4 was only observed when all follicle classes of an individual were expressing both FGF-8 and FGFR-3c. We conclude that FGF-8 and its receptors are expressed in preantral follicles in a developmentally regulated manner. (C) 2005 Wiley-Liss, Inc.

Gluconeogenesis and P-enolpyruvate carboxykinase in liver and kidney of long-term fasted quails

The activity of cytoplasmic and mitochondrial phosphoenolpyruvate carboxykinase (PEPCK) in kidney and liver, and in vivo gluconeogenic activity, were determined during different phases of prolonged fasting in quails. The fasting-induced changes in the activity of kidney cytoplasmic PEPCK were positively correlated with the changes in gluconeogenesis. Both activities increased at the initial phase (I) of fasting to levels 65% to 100% higher than fed values, and decreased during the protein-sparing period (phase II), although remaining higher than in fed birds. At the catabolic final phase (III) both kidney cytoplasmic PEPCK activity and gluconeogenesis increased markedly, attaining levels 115% to 150% higher than fed values. The activity of liver cytoplasmic PEPCK, present in appreciable amounts in quails, did not change during phases I and II of fasting, but increased to levels 60% higher than fed values at the final phase (III). Plasma glucose levels at phase III did not differ significantly from those at phases I and II. In both kidney and liver the activity of the mitochondrial PEPCK was not significantly affected by fasting. The data suggest that the kidney cytoplasmic PEPCK is the main enzyme responsible for gluconeogenesis adjustments during food deprivation in quails, and that this function is complemented at the final phase by enzyme present in liver cytosol.

Maternal undernutrition and the offspring kidney: from fetal to adult life

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Analytical approach to the metallomic of Nile tilapia (Oreochromis niloticus) liver tissue by SRXRF and FAAS after 2D-PAGE separation: Preliminary results

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cytotoxic effects of permethrin on mouse liver and spleen cells

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Action of the chemical agent fipronil (active ingredient of acaricide Frontline (R)) on the liver of mice: An ultrastructural analysis

Fipronil, active ingredient of the acaricide Frontiline (R), is a phenyl-pyrazolic derivative, and its efficacy in the elimination of several plagues, even in low concentrations, has already been demonstrated; however, its effect on nontarget organisms has not been thoroughly explained. In this sense, the objective of this study was to evaluate the effects of different dosages of fipronil on the liver of mice in artificial conditions. Results showed that the animals exposed to fipronil present significant ultrastrucutural changes in hepatic cells with evident cellular and cytoplasm disorganization in hepatocytes characterized by an increase in the number of organelles, mainly mitochondria and rough endoplasmic reticulum, organelles that, in the case of the exposed animals, were probably responsible for the enzymes' synthesis that have the function of inactivating the toxic metabolites. A fat accumulation in the hepatocytes' cytoplasm (steatosis) was observed, in addition to extended vacuolated areas, mainly in regions next to the cell nucleus. Alterations observed in the nuclei of the hepatocytes pointed out cell death processes. Moreover, Kupffer cells increased in number (hyperplasia) suggesting an increase in the phagocytic activity of the liver in the exposed animals. Microsc. Res. Tech., 2011. (c) 2011 Wiley Periodicals, Inc.

Cytotoxicity of fipronil on mice liver cells

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of short-term physical training on the liver IGF-I in diabetic rats

To investigate the influence of short-term physical training on IGF-I concentrations in diabetic rats, male wistar rats were distributed into four groups: sedentary control, trained control, sedentary diabetic and trained diabetic. Diabetes was induced by Alloxan (32 mg/kg b.w.) and training protocol consisted of swimming 1 h/day, 5 days/week, during 4 weeks, supporting 5% b.w. At the end of this period, rats were sacrificed and blood was collected for determinations of serum glucose, insulin, albumin, IGF-I and hematocrit. Liver samples were used to determine glycogen, protein, DNA and IGF-I concentrations. Diabetes reduced insulin and IGF-I concentrations in blood and liver protein, ratio protein/DNA and IGF-I concentrations in liver and increased glycemia. Physical training reduced serum glucose and recovered hepatic glycogen stores in diabetic rats and reduced serum and liver IGF-I concentrations. In conclusion, short-term physical training improved the metabolic conditions of diabetic rats, despite of impairing liver and blood IGF-I concentrations.

Development of the insulin secretion mechanism in fetal and neonatal rat pancreatic B-cells: response to glucose, K+, theophylline, and carbamylcholine

We studied the development of the insulin secretion mechanism in the pancreas of fetal (19- and 21-day-old), neonatal (3-day-old), and adult (90-day-old) rats in response to stimulation with 8.3 or 16.7 mM glucose, 30 mM K+, 5 mM theophylline (Theo) and 200 µM carbamylcholine (Cch). No effect of glucose or high K+ was observed on the pancreas from 19-day-old fetuses, whereas Theo and Cch significantly increased insulin secretion at this age (82 and 127% above basal levels, respectively). High K+ also failed to alter the insulin secretion in the pancreas from 21-day-old fetuses, whereas 8.3 mM and 16.7 mM glucose significantly stimulated insulin release by 41 and 54% above basal levels, respectively. Similar results were obtained with Theo and Cch. A more marked effect of glucose on insulin secretion was observed in the pancreas of 3-day-old rats, reaching 84 and 179% above basal levels with 8.3 mM and 16.7 mM glucose, respectively. At this age, both Theo and Cch increased insulin secretion to close to two-times basal levels. In islets from adult rats, 8.3 mM and 16.7 mM glucose, Theo, and Cch increased the insulin release by 104, 193, 318 and 396% above basal levels, respectively. These data indicate that pancreatic B-cells from 19-day-old fetuses were already sensitive to stimuli that use either cAMP or IP3 and DAG as second messengers, but insensitive to stimuli such as glucose and high K+ that induce membrane depolarization. The greater effect of glucose on insulin secretion during the neonatal period indicates that this period is crucial for the maturation of the glucose-sensing mechanism in B-cells.

Aerobic capacity of rats recovered from fetal malnutrition with a fructose-rich diet

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Long-term physical training increases liver IGF-I in diabetic rats

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Changes of glycogen content in liver, skeletal muscle, and heart from fasted rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Exercise counteracts fatty liver disease in rats fed on fructose-rich diet

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Fructose-rich diet leads to reduced aerobic capacity and to liver injury in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)