Craving em alcoolistas e sua relação com a escolha de alimentos / Craving in alcoholics and its relation to food choices

Introdução: Em alcoolistas crônicos, durante a fase de abstinência, pode surgir o craving ou fissura, desejo intenso de usar a substância, podendo estar associado ao aumento do desejo de consumir alimentos doces para diminuir sintomas da abstinência. Assim, o objetivo principal deste estudo foi avaliar a presença do craving, associando-o à escolha de alimentos em indivíduos alcoolistas, internos para desintoxicação. Metodologia: O presente estudo é do tipo transversal, descritivo e quantitativo, desenvolvido com 40 internos, com idade entre 20 e 66 anos em uma Instituição hospitalar no interior de Pernambuco- Brasil.  Foram analisados aspectos sociodemográficos e o estado nutricional dos envolvidos. Também foram utilizados questionários específicos para avaliação do craving e hábitos alimentares dos alcoolistas. Resultados e Discussão: Foram identificados hábitos alimentares inadequados, como alto consumo de embutidos (77,5%) e baixo consumo de frutas e hortaliças (52,5%), além de um percentual elevado de desnutrição proteica nos avaliados. Verificou-se que 25% (n= 10) dos pacientes estudados apresentaram craving moderado a forte. Foi possível observar que 27,5% dos indivíduos relataram sentir vontade de consumir alimentos fontes de carboidratos simples, para desviar o pensamento no consumo da bebida alcoólica. Conclusão: Foi identificado que parte da amostra estudada apresentou craving moderado a forte e um desejo de consumir alimentos ricos em carboidratos no intuito e desviar o craving, contudo, a partir das análises estatísticas, não foi verificado associação entre o craving e o consumo de alimentos ricos em carboidratos, devendo-se realizar mais estudos para conhecimento desta relação. No entanto, quanto ao consumo alimentar, foi demonstrado a necessidade de melhores orientações nutricionais como parte do tratamento multiprofissional na assistência à saúde destes indivíduos

Efeitos da exposi??o de ratos ? dieta hiperlip?dica sobre par?metros cardiometab?licos das proles F1 e F2.

Programa de P?s-Gradua??o em Ci?ncias Biol?gicas. N?cleo de Pesquisas em Ci?ncias Biol?gicas, Pr?-Reitoria de Pesquisa de P?s Gradua??o, Universidade Federal de Ouro Preto.A m? alimenta??o dos progenitores pode predispor a prole a doen?as cardiometab?licas. O objetivo desse estudo foi investigar se a dieta hiperlip?dica (H) submetida aos progenitores predisp?e a prole a dist?rbios cardiometab?licos. Para isso ratos Fischer foram submetidos ? dieta H (G0HM e G0HF) ou controle (C) (G0CM e G0CF) durante o acasalamento, gesta??o e lacta??o, gerando as proles F1 (F1HM e F1CM) ou (F1HF e F1CF). Parte das proles F1 (F1HM e F1CM) ou (F1HF e F1CF) foram acasalados e tornaram-se os genitores G1 (G1HM e G1HF) ou (G1CM e G1CF), e suas proles divididas em (F2HM e F2CM) ou (F2HF e F2CF). Todas as proles F1 e F2 consumiram dieta C ap?s desmame at? completar 90 dias de idade. Avaliou-se os par?metros nutricionais, biom?tricos, bioqu?micos e hemodin?micos. Os progenitores G0HM apresentaram aumento da PAM (PAM), FC (bpm) e massa corporal (g). As progenitoras apresentaram resist?ncia ? insulina (ng/ml), aumento do ?ndice de adiposidade, dos n?veis de triglic?rides (mg/dL), da ingesta energ?tica (Kcal), aumento relativo do p?ncreas (g/100g), da glicemia (mg/dL), do HOMA-IR e da PAM. Os ratos F1HM (n=6-14) e F1HF (n= 6-9) apresentaram aumento da PAM (123?4 e 122?3; respectivamente), maior queda da PAM induzida pelo hexamet?nio (ms/mmHg) (-56?2 e -44?5; respectivamente), da ingesta de ?gua (ml) (238?12 e 164?8; respectivamente), ingesta cal?rica (791?12 e 587?11; respectivamente) e alimentar (g) (226?5 e 168?6; respectivamente), o dep?sito de gordura retroperitoneal (g/100g) (5,9?4 e 5,0?0,3; respectivamente), o ?ndice de adiposidade (18?1,4 e 7?0,4; respectivamente), a massa corporal (341?1 e 218?5; respectivamente), a glicemia de jejum (138?2 e 129?4; respectivamente), e triglic?rides (176?10 e 180?10; respectivamente) comparado aos grupos F1CM (n=6-16) e F1CF (n=6-18). Os ratos F2HM (n=7-12) e F2HF (8-15) apresentaram aumento a PAM (127?1 e 130?5; respectivamente), maior queda da PAM induzida pelo hexamet?nio (-46?1 e -42?2; respectivamente), a ingesta de ?gua (257?10 e 188?8; respectivamente), ingesta alimentar (233?7 e 176?6; respectivamente) e cal?rica (812?13 e 608?12; respectivamente), peso relativo do f?gado (g/100g) (3,4?0,1 e 3,5?0,1; respectivamente), o ?ndice de adiposidade (13?0,2 e 7,7?0,1; respectivamente), massa corporal (336?3 e 209?2; respectivamente), a glicemia de jejum (124?2 e 123?7; respectivamente), o colesterol total (mg/dL) (93?2 e 103?3; respectivamente) e os triglic?rides (142?8 e 169?9; respectivamente) comparado aos grupos F2CM (n= 8-11) e F2CF (n=8-12). Nossos dados mostram que a dieta H materna durante o acasalamento, gesta??o e lacta??o induziu dist?rbios caracter?sticos da SM nas proles F1 e F2 mesmo estas sendo alimentadas com dieta C ap?s desmame. Al?m disso, esses dist?rbios cardiometab?licos foram de maior extens?o nas proles F2 em rela??o as proles F1.The poor maternal diet during pregnancy can predispose the offspring to cardiometabolic diseases. The aim of this study was to investigate whether the high fat diet (H) submitted to parents predisposes the offspring to cardiometabolic disorders. For this, Fischer rats were submitted to diet H (G0HM and G0HF) or control (C) (G0CM and G0CF) during mating, gestation and lactation, generating F1 (F1HM and F1CM) or (F1HF and F1CF) offspring. Part of the F1 (F1HM and F1CM) or (F1HF and F1CF) progeny were mated and became the G1 (G1HM and G1HF) or (G1CM and G1CF) parents, and their offspring divided into (F2HM and F2CM) or (F2HF and F2CF). All F1 and F2 offspring consumed C diet after weaning until 90 days of age. Nutritional, biometric, biochemical and hemodynamic parameters were evaluated. The G0HM progenitors presented increase of mean arterial pressure (MAP-mmHg), FC (bpm) and body mass (g). The progenitors presented insulin resistance (ng / ml), increase in the adiposity index, triglyceride levels (mg / dL), energy intake (Kcal), relative increase of pancreas (g / 100g) dL), HOMA-IR and MAP.The F1HM (n = 6-14) and F1HF (n = 6-9) rats presented an increase in MAP (123 ? 4 and 122 ? 3, respectively), a higher fall in MAP induced by hexamethonium (ms/mmHg) (-56?2 and -44?5,respectively), and ingestion of water (ml) (238?12 and 164?8, respectively), caloric intake (791?12 and 587?5, respectively), the retroperitoneal fat deposit (g / 100g) (5.9?4 and 5.0?0.3, respectively), the adiposity index (18?1.4 and 7?0,4, respectively), body mass (341?1 and 218 ? 5, respectively), fasting glycemia (138?2 and 129?4, respectively), and triglycerides (176?10 and 180?10; respectively) compared to F1CM (n =6-16) and F1CF (n =6-18) groups. The F2HM (n=7-12) and F2HF (8-15) rats showed an increase in MAP (127?1 and 130? 5, respectively), a higher fall in MAP-induced by hexamethonium (-46?1 and -42?2, respectively), ingestion of water (257?10 and 188?8, respectively), food ingestion (233?7 and 174?6, respectively) and caloric intake (812?13 vs 608?12, respectively), relative weight of the liver (g / 100g) (3.4?0.1 vs 3.5?0.1, respectively), adiposity index (13?0.2 and 7.7?0.1, respectively), body mass (123?2 and 123?7, respectively), total cholesterol (mg / dL) (93? 2 and 103?3, respectively) and the total cholesterol (336 ? 3 and 209 ? 2, respectively), fasting glycemia (142?8 and 169?9, respectively) compared to F2CM (n=8-11) and F2CF (n=8-12) groups. Our data show that the maternal H diet during mating, gestation and lactation induced characteristic disturbances of MS in F1 and F2 offspring even though they were fed C diet after weaning. In addition, these cardiometabolic disorders were of greater extension in the F2 offspring relative to the F1 offspring

Maternal high-fat diet triggers metabolic syndrome disorders that are transferred to first and second offspring generations.

A high-fat (H) diet increases metabolic disorders in offspring. However, there is great variability in the literature regarding the time of exposure, composition of the H diets offered to the genitors and/or offspring and parameters evaluated. Here, we investigated the effect of a H diet subjected to the genitors on different cardio-metabolic parameters on first (F1)- and second (F2)-generation offspring. Female Fischer rats, during mating, gestation and breast-feeding, were subjected to the H diet (G0HF) or control (G0CF) diets. Part of F1 offspring becomes G1 genitors for generating the F2 offspring. After weaning, F1 and F2 rats consumed only the C diet. Nutritional, biometric, biochemical and haemodynamic parameters were evaluated. G0HF genitors had a reduction in food intake but energy intake was similar to the control group. Compared with the control group, the F1H and F2H offspring presented increased plasma leptin, insulin and fasting glucose levels, dietary intake, energy intake, adiposity index, mean arterial pressure, sympathetic drive evidenced by the hexamethonium and insulin resistance. Our data showed that only during mating, gestation and breast-feeding, maternal H diet induced cardio-metabolic disorders characteristic of human metabolic syndrome that were transferred to both females and males of F1 and F2 offspring, even if they were fed control diet after weaning. This process probably occurs due to the disturbance in mechanisms related to leptin that increases energy intake in F1H and F2H offspring. The present data reinforce the importance of balanced diet during pregnancy and breast-feeding for the health of the F1 and F2 offspring

Hypotensive effect induced by microinjection of Alamandine, a derivative of angiotensin-(1?7), into caudal ventrolateral medulla of 2K1C hypertensive rats.

In the present study we evaluated the cardiovascular effects produced by microinjection of the new component of the renin-angiotensin system, alamandine, into caudal ventrolateral medulla of urethane-anesthetized normotensive and hypertensive 2K1C rats. The participation of different angiotensin receptors in the effects of alamandine was also evaluated. Microinjection of angiotensin-(1?7) was used for comparison. The microinjection of 4, 40 and 140 pmol of alamandine or angiotensin-(1?7) into caudal ventrolateral medulla induced similar hypotensive effects in Sham-operated rats. However, contrasting with angiotensin-(1?7), in 2K1C rats the MAP response to the highest dose of alamandine was similar to that observed with saline. The microinjection of A- 779, a selective Mas receptor antagonist, blunted the angiotensin-(1?7) effects but did not block the hypotensive effect of alamandine in Sham or in 2K1C rats. However, microinjection of D-Pro7-angiotensin-(1?7), a Mas/MrgD receptor antagonist, blocked the hypotensive effect induced by both peptides. Furthermore, microinjection of PD123319, a putative AT2 receptor antagonist blocked the hypotensive effect of alamandine, but not of angiotensin-( 1?7), in Sham and 2K1C rats. Microinjection of the AT1 receptor antagonist, losartan, did not alter the hypotensive effect of angiotensin-(1?7) or alamandine in both groups. These results provide new insights about the differential mechanisms participating in the central cardiovascular effects of alamandine and angiotensin- (1?7) in normotensive and 2K1C hypertensive rats

Discovery and Characterization of Alamandine, a Novel Component of the Renin-Angiotensin System

The renin?angiotensin system (RAS) is a key regulator of the cardiovascular system, electrolyte, and water balance. Here, we report identification and characterization of alamandine, a new heptapeptide generated by catalytic action of angiotensin-converting enzyme-2 angiotensin A or directly from angiotensin-(1?7). To characterize a novel component of the RAS, alamandine. Using mass spectrometry we observed that alamandine circulates in human blood and can be formed from angiotensin-(1?7) in the heart. Alamandine produces several physiological actions that resemble those produced by angiotensin-(1?7), including vasodilation, antifibrosis, antihypertensive, and central effects. Interestingly, our data reveal that its actions are independent of the known vasodilator receptors of the RAS, Mas, and angiotensin II type 2 receptor. Rather, we demonstrate that alamandine acts through the Mas-related G-protein?coupled receptor, member D. Binding of alamandine to Mas-related G-protein?coupled receptor, member D is blocked by D-Pro7-angiotensin-(1?7), the Mas-related G-protein?coupled receptor, member D ligand ?-alanine and PD123319, but not by the Mas antagonist A-779. In addition, oral administration of an inclusion compound of alamandine/?-hydroxypropyl cyclodextrin produced a long-term antihypertensive effect in spontaneously hypertensive rats and antifibrotic effects in isoproterenol-treated rats. Alamandine had no noticeable proliferative or antiproliferative effect in human tumoral cell lines. The identification of these 2 novel components of the RAS, alamandine and its receptor, provides new insights for the understanding of the physiological and pathophysiological role of the RAS and may help to develop new therapeutic strategies for treating human cardiovascular diseases and other related disorders