Introduction: Evidences suggest that fat intake, visceral obesity and intracellular lipids are related to insulin impairment. Objective: The objective of the present paper was correlate visceral obesity and metabolic alterations in control (CTR) and hyperlipidic cafeteria diet (CFT) fed animals. Methods: After 6 months of diet treatment, liver and muscle of the male rats were utilized to determined glucose uptake and glycogen metabolism after administration of 0.4I U/kg insulin in vivo, and correlate the visceral adiposity to these two parameters. Results: Ample range of physiologic answers to body composition in metabolic profile of the both diets was found. No differences were found in glycemia and triacylglycerol after insulin action in both groups, however CFT group accumulated higher adiposity, mostly visceral fat, and showed lower glycogen content in the liver. We also found an inverse correlation between visceral adiposity and glucose uptake and a decrease of the glycogen synthase active form in the liver. CTR animals demonstrated an inverse correlation between glucose uptake and visceral adiposity in the muscle. Discussion and conclusion: It was observed a variability of metabolic alterations in animals which can be related to degree of accumulation of abdominal adiposity and ingestion of diet fats. Further studies will be required to clarify the reasons for the observed liver alterations in CFT and muscle alterations in CTR animals.

Introducción: Las evidencias sugieren que la ingesta de grasas, obesidad visceral y lípidos intracelulares están relacionados con resistencia a la acción de la insulina. Objetivo: El objetivo del presente trabajo fue correlacionar la obesidad visceral con alteraciones metabólicas en los animales controles (CTR) y alimentados con la dieta de cafeteria hiperlipidica (CFT). Metodos: Después de 6 meses de tratamiento con dieta, el hígado y lo musculo esqueletico de los ratones se utilizaron para determinar la captación de glucosa y el metabolismo del glucógeno después de la administración de la insulina 0.4 UI/kg in vivo y correlacionar la adiposidad visceral a estos dos parámetros. Resultados: Una amplia gama de respuestas fisiológicas a la composición corporal era encontrado. No se encontraron diferencias en la glucemia y triglicéridos después de la acción de la insulina en ambos grupos, sin embargo CFT grupo acumuló mayor adiposidad, principalmente adiposidad visceral, y mostraron menor contenido de glucógeno en el hígado. También se encontró una correlación inversa entre la adiposidad visceral y la captación de glucosa y una disminución de la forma activa de la enzima glucógeno sintasa en el hígado. Animales CTR demostrado una correlación inversa entre la captación de glucosa y la adiposidad visceral en el músculo. Discusión y conclusiones: Se observó una gran variabilidad de alteraciones metabólicas en los animales que se pueden relacionados con las tasas de acumulación de la adiposidad visceral y la ingestión de grasas dietéticas. Más estudios serán necesarios para aclarar las razones de las alteraciones observadas en el hígado de los animales CFT y las alteraciones musculares en animales CTR.

FUNDAMENTO: A ressuscitação de parada cardíaca pode apresentar disfunção miocárdica determinada pelo tempo da isquemia, e a inibição da enzima conversora de angiotensina (ECA) pode reduzir a disfunção cardíaca durante a reperfusão. OBJETIVO: Investigar os efeitos da angiotensina-I e diferentes períodos de isquemia na recuperação funcional em corações de ratos isolados. MÉTODOS: Os corações isolados de ratos Wistar (n = 45; 250-300 g) foram submetidos a diferentes períodos de isquemia global (20, 25 ou 30 min) e reperfundidos (30 min) com o tampão Krebs-Henseleit, ou com a adição de 400 nmol/L de angiotensina-I, ou com 400 nmol/L de angiotensina-I + 100 µmol/L de captopril durante o período de reperfusão. RESULTADOS: A derivada positiva máxima de pressão (+dP/dt max) e o produto frequência-pressão foram reduzidos nos corações expostos à isquemia de 25 min (~ 73%) e à isquemia de 30 min (~ 80%) vs. isquemia de 20 min. A pressão diastólica final do ventrículo esquerdo (PDFVE) e a pressão de perfusão (PP) foram aumentadas nos corações expostos à isquemia de 25 min (5,5 e 1,08 vezes, respectivamente) e à isquemia de 30 min (6 e 1,10 vezes, respectivamente) vs. isquemia de 20 min. A angiotensina-I ocasionou uma diminuição no +dP/dt max e no produto frequência-pressão (~ 85-94%) em todos os períodos de isquemia e um aumento na PDFVE e na PP (6,9 e 1,25 vezes, respectivamente) apenas na isquemia de 20 min. O captopril foi capaz de reverter parcial ou completamente os efeitos da angiotensina-I na recuperação funcional nas isquemias de 20 e 25 min CONCLUSÃO: Os dados sugerem que a angiotensina-II participa direta ou indiretamente no dano pós-isquêmico e que a capacidade de um inibidor da ECA atenuar esse dano depende do tempo de isquemia.

BACKGROUND: Cardiac arrest resuscitation can present myocardial dysfunction determined by ischemic time, and inhibition of the angiotensin-converting enzyme (ACE) can reduce cardiac dysfunction during reperfusion. OBJECTIVE: To investigate the effects of angiotensin-I and different periods of ischemia on functional recovery in isolated rat hearts. METHODS: Isolated hearts from Wistar rats (n=45; 250-300 g) were submitted to different periods of global ischemia (20, 25 or 30 min) and reperfused (30 min) with Krebs-Henseleit buffer alone or with the addition of 400 nmol/L angiotensin-I, or 400 nmol/L angiotensin-I + 100 mmol/L captopril along the reperfusion period. RESULTS: The maximal positive derivative of pressure (+dP/dt max) and rate-pressure product were reduced in hearts exposed to 25 min ischemia (~73%) and 30 min ischemia (~80%) vs. 20 min ischemia. Left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP) were increased in hearts exposed to 25 min ischemia (5.5 and 1.08 fold, respectively) and 30 min ischemia (6 and 1.10 fold, respectively) vs. 20 min ischemia. Angiotensin-I caused a decrease in +dP/dt max and rate-pressure product (~85-94%) in all ischemic periods and an increase in LVEDP and PP (6.9 and 1.25 fold, respectively) only at 20 min ischemia. Captopril was able to partially or completely reverse the effects of angiotensin-I on functional recovery in 20 min and 25 min ischemia. CONCLUSION: These data suggest that angiotensin-II directly or indirectly participates in the post-ischemic damage, and the ability of an ACE inhibitor to attenuate this damage depends on ischemic time.

In this paper, two methods for assessing the degree of melanization of pupal exuviae from the butterfly Heliconius erato phyllis , Fabricius 1775 (Lepidoptera, Nymphalidae, Heliconiini) are compared. In the first method, which was qualitative, the exuviae were classified by scoring the degree of melanization, whereas in the second method, which was quantitative, the exuviae were classified by optical density followed by analysis with appropriate software. The heritability (h 2 ) of the degree of melanization was estimated by regression and analysis of variance. The estimates of h 2 were similar with both methods, indicating that the qualitative method could be particularly suitable for field work. The low estimates obtained for heritability may have resulted from the small sample size ( n = 7-18 broods, including the parents) or from the allocation-priority hypothesis in which pupal color would be a lower priority trait compared to morphological traits and adequate larval development.