Effects of Taenia Pisiformis Infection and Obesity on Clinical Parameters, Organometry and Fat Distribution in Male Rabbits.

Taenia pisiformis infection causes important economic loss in farms. It is suggested that obesity has a major impact on infection and reproduction. We addressed the impact of T. pisiformis infection in normal and obese rabbits to evaluate its effect on parameters important in behavior and reproduction. T. pisiformis infection in obese rabbits decreased body weight. In the obese-infected rabbits, eosinophils and heterophiles were increased 23% by the infection (P ≤ 0.05). T. pisiformis decreased cholesterol by 13% in normal weight infected rabbits and 10% in obese group (P ≤ 0.05), while triglyceride and VLDL were increased by 23% and 45% in the non-infected obese group (P ≤ 0.05). The infection increased serum cortisol levels only in normal weight rabbits (P ≤ 0.05). Liver weight was 20% higher in obese and obese-infected rabbits (P ≤ 0.05). Testicular weight in obese-infected was 46% higher than normal weight (P ≤ 0.0001) and 20% more than the obese-non-infected (P ≤ 0.0001). Furthermore, the infection reduced the weight of submandibular glands in infected and obese-infected rabbits (P ≤ 0.05), body fat increased 10% in the obese-infected than in the obese, and infected group was 35% over the normal weight non-infected (P ≤ 0.01). Our results show that T. pisiformis alters metabolic characteristics in rabbits, which can impact on the production and welfare of animals.

Involvement of Melatonin in the Regulation of the Circadian System in Crayfish.

Melatonin (MEL) is an ancient molecule, broadly distributed in nature from unicellular to multicellular species. MEL is an indoleamine that acts on a wide variety of cellular targets regulating different physiological functions. This review is focused on the role played by this molecule in the regulation of the circadian rhythms in crayfish. In these species, information about internal and external time progression might be transmitted by the periodical release of MEL and other endocrine signals acting through the pacemaker. We describe documented and original evidence in support of this hypothesis that also suggests that the rhythmic release of MEL contributes to the reinforcement of the temporal organization of nocturnal or diurnal circadian oscillators. Finally, we discuss how MEL might coordinate functions that converge in the performance of complex behaviors, such as the agonistic responses to establish social dominance status in Procambarus clarkii and the burrowing behavior in the secondary digging crayfish P. acanthophorus.

Circadian rhythm in melatonin release as a mechanism to reinforce the temporal organization of the circadian system in crayfish.

Melatonin (MEL) is a conserved molecule with respect to its synthesis pathway and functions. In crayfish, MEL content in eyestalks (Ey) increases at night under the photoperiod, and this indoleamine synchronizes the circadian rhythm of electroretinogram amplitude, which is expressed by retinas and controlled by the cerebroid ganglion (CG). The aim of this study was to determine whether MEL content in eyestalks and CG or circulating MEL in hemolymph (He) follows a circadian rhythm under a free-running condition; in addition, it was tested whether MEL might directly influence the spontaneous electrical activity of the CG. Crayfish were maintained under constant darkness and temperature, a condition suitable for studying the intrinsic properties of circadian systems. MEL was quantified in samples obtained from He, Ey, and CG by means of an enzyme-linked immunosorbent assay, and the effect of exogenous MEL on CG spontaneous activity was evaluated by electrophysiological recording. Variation of MEL content in He, Ey, and CG followed a circadian rhythm that peaked at the same circadian time (CT). In addition, a single dose of MEL injected into the crayfish at different CTs reduced the level of spontaneous electrical activity in the CG. Results suggest that the circadian increase in MEL content directly affects the CG, reducing its spontaneous electrical activity, and that MEL might act as a periodical signal to reinforce the organization of the circadian system in crayfish.

Neuroendocrine cells are present in the domestic fowl ovary.

Neuroendocrine cells are present in virtually all organs of the vertebrate body; however, it is yet uncertain whether they exist in the ovaries. Previous reports of ovarian neurons and neuron-like cells in mammals and birds might have resulted from misidentification. The aim of the present work was to determine the identity of neuron-like cells in immature ovaries of the domestic fowl. Cells immunoreactive to neurofilaments, synaptophysin, and chromogranin-A, with small, dense-core secretory granules, were consistently observed throughout the sub-cortical ovarian medulla and cortical interfollicular stroma. These cells also displayed immunoreactivity for tyrosine, tryptophan and dopamine ß-hydroxylases, as well as to aromatic L-DOPA decarboxylase, implying their ability to synthesize both catecholamines and indolamines. Our results support the argument that the ovarian cells previously reported as neuron-like in birds, are neuroendocrine cells.

EphB4 is developmentally and differentially regulated in blood vessels throughout the forebrain neurogenic niche in the mouse brain: Implications for vascular remodeling.

Neurogenesis is a process influenced by environmental cues that create highly specific functional niches. Recently, the role of blood vessels in the maintenance and functioning of neurogenic niches during development and in adult life has been hallmarked. In addition to their trophic support for the highly demanding neurogenic process, blood vessels regulate neuroblast differentiation and migration and define functional domains. Since neurogenesis along the forebrain neurogenic niche (FNN) is a multistage process, in which neuroblast proliferation, differentiation and migration are spatially restricted to specific locations; we evaluated the structural features of vascular beds that support these processes during critical time points in their development. Additionally, we studied the molecular identity of the endothelial components of vascular beds using the expression of the venous marker EphB4. Our results show that blood vessels along the FNN: 1) are present very early in development; 2) define the borders of the FNN since early developmental stages; 3) experience constant remodeling until achieving their mature structure; 4) show venous features during perinatal developmental times; and 5) down-regulate their EphB4 expression as development proceeds. Collectively, our results describe the formation of the intricate vascular network that may support neurogenesis along the FNN and show that blood vessels along this neurogenic niche are dynamic entities that experience significant structural and molecular remodeling throughout development.

Biotin deficiency and biotin excess: effects on the female reproductive system.

Biotin deficiency and biotin excess have both been found to affect reproduction and cause teratogenic effects. In the reproductive tract, however, the effects of biotin have not been well established yet. We investigated the effects of varying biotin content diets on the oestrus cycle, ovarian morphology, estradiol and progesterone serum levels, and the uterine mRNA abundance of their nuclear receptors, as well as on the activity of the estradiol-degrading group of enzymes cytochrome P450 (CYP) in the liver. Three-week-old female BALB/cAnN Hsd mice were fed a biotin-deficient, a biotin-control, or a biotin-supplemented diet (0, 7.2 or 400 micromol of free biotin/kg diet, respectively) over a period of nine weeks. Striking effects were observed in the biotin-deficient group: mice showed arrested estrous cycle on the day of diestrus and changes in ovary morphology. Estradiol serum concentration increased 49.2% in biotin-deficient mice compared to the control group, while the enzymatic activities of CYP1A2 and CYP2B2 increased (P<0.05). The mRNA abundance of nuclear estrogen and progesterone receptors decreased in the biotin-deficient mice. In the biotin-supplemented group we found that, in spite of a significant (P<0.05) decrease in the number of primary and Graafian follicles and in CYP1A2 activities, mice exhibited 105.4% higher serum estradiol concentration than the control group. No changes in the expression of the nuclear receptors were observed. No significant differences were observed in serum progesterone among the groups. Our results indicate that both the deficiency and the excess of biotin have significant effects on the female mouse reproductive system.

Brain plasticity, signal transduction and epigenesis: a missing link revealed

It has been long thought that the brain reorganizes itself in response to environmental needs. Sensory experiences coded in action potentials are the mean by which information on the surroundings is introduced into neuronal networks. The information approaching the brain in the form of electrochemical codes must then be translated in biochemical, epigenetic and genetic ones. Only until recently we have begun understanding the underpinning of such informational transformations and how this process is expressed as neuronal plastic responses. Central for our comprehension of this matter is the finding that signals transduction cascades can modify gene expression by remodeling the chromatin through epigenetic mechanisms. Hence, chromatin remodeling seems to be the process by which experiences are “imprinted”.

Biotin supplementation reduces plasma triacylglycerol and VLDL in type 2 diabetic patients and in nondiabetic subjects with hypertriglyceridemia.

Biotin is a water-soluble vitamin that acts as a prosthetic group of carboxylases. Besides its role as carboxylase prosthetic group, biotin regulates gene expression and has a wide repertoire of effects on systemic processes. The vitamin regulates genes that are critical in the regulation of intermediary metabolism. Several studies have reported a relationship between biotin and blood lipids. In the present work we investigated the effect of biotin administration on the concentration of plasma lipids, as well as glucose and insulin in type 2 diabetic and nondiabetic subjects. Eighteen diabetic and 15 nondiabetic subjects aged 30-65 were randomized into two groups and received either 61.4 micromol/day of biotin or placebo for 28 days. Plasma samples obtained at baseline and after treatment were analyzed for total triglyceride, cholesterol, very low density lipoprotein (VLDL), glucose and insulin. We found that the vitamin significantly reduced (P=0.005) plasma triacylglycerol and VLDL concentrations. Biotin produced the following changes (mean of absolute differences between 0 and 28 day treatment+/-S.E.M.): a) triacylglycerol -0.55+/-0.2 in the diabetic group and -0.92+/-0.36 in the nondiabetic group; b) VLDL: -0.11+/-0.04 in the diabetic group and -0.18+/-0.07 in the nondiabetic group. Biotin treatment had no significant effects on cholesterol, glucose and insulin in either the diabetic or nondiabetic subjects. We conclude that pharmacological doses of biotin decrease hypertriglyceridemia. The triglyceride-lowering effect of biotin suggests that biotin could be used in the treatment of hypertriglyceridemia.

Effects of biotin on pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and markers for glucose and lipid homeostasis in type 2 diabetic patients and nondiabetic subjects.

BACKGROUND: Several studies have shown that biotin affects glucose homeostasis. Serum biotin concentrations are lower in subjects with type 2 diabetes than in control subjects. Lymphocyte propionyl-CoA carboxylase (PCC; EC 6.4.1.3) activity has proved to be a sensitive indicator of biotin status that is more accurate than is serum biotin concentration. OBJECTIVE: We studied the activity of PCC, pyruvate carboxylase (PC; EC 6.4.1.1), and acetyl-CoA carboxylase (ACC; EC 6.4.1.2) in type 2 diabetic and nondiabetic subjects. The effect of biotin administration (6.14 micro mol/d) on the activity of these enzymes and on several plasma metabolites was also studied. DESIGN: We compared the activities of carboxylases in circulating lymphocytes from patients with type 2 diabetes (n = 24) with those in circulating lymphocytes from nondiabetic subjects (n = 30). We also assessed the effect of biotin administration for 14 and 28 d on the activity of these enzymes and on the concentrations of several metabolites (type 2 diabetic patients, n = 10; nondiabetic subjects, n = 7). RESULTS: No significant differences in lymphocyte carboxylase activities were found between the type 2 diabetic patients and the nondiabetic subjects. Biotin administration increased the activity of PCC, PC, and ACC in all the subjects. No significant change in glucose, insulin, triacylglycerol, cholesterol, or lactate concentration was observed with the treatment in either the diabetic or the nondiabetic subjects. CONCLUSIONS: The activity of carboxylases does not differ significantly between type 2 diabetic and nondiabetic subjects. Pharmacologic doses of biotin increase lymphocyte PCC, PC, and ACC activities.