Effect of remote ischemic preconditioning in the expression of IL-6 and IL-10 in a rat model of liver ischemia-reperfusion injury.

PURPOSE: To study the effect of remote ischemic preconditioning (RIPC) in ischemia-reperfusion (I/R) liver injury and in the expression of IL-6 and IL-10 in a rat model. METHODS: Thirty-six male rats were divided in three groups: Sham; I/R injury, a 45 minutes lobar liver ischemia and reperfusion; and RIPC, six cycles of four minutes of ischemia and four minutes of reperfusion on the right hindlimb followed by a 45 minutes lobar liver ischemia and reperfusion. Tissue and blood samples were collected after 1h and 3h of reperfusion for histopathological study, plasma cytokines and alanine aminotransferase (ALT) measurement. RESULTS: The histopathological study demonstrated a significant reduction in liver necrosis in the RIPC group (p<0,001). The ALT levels were also significant lower in the RIPC group (p<0.01). The cytokines assessment showed that IL-6 levels were increased in the RIPC group after 1h of reperfusion, in comparison to the I/R group (p<0.05). Interleukin-10 levels in RIPC groups did not differ significantly from I/R group. CONCLUSIONS: Remote ischemic preconditioning is effective in decreasing liver necrosis in a rat model of ischemia-reperfusion. The IL-6 expression is up-regulated and peaked at 60 min of reperfusion. There was no difference in IL-10 expression between the groups.

Effect of remote ischemic preconditioning in the expression of IL-6 and IL-10 in a rat model of liver ischemia-reperfusion injury

PURPOSE: To study the effect of remote ischemic preconditioning (RIPC) in ischemia-reperfusion (I/R) liver injury and in the expression of IL-6 and IL-10 in a rat model. METHODS: Thirty-six male rats were divided in three groups: Sham; I/R injury, a 45 minutes lobar liver ischemia and reperfusion; and RIPC, six cycles of four minutes of ischemia and four minutes of reperfusion on the right hindlimb followed by a 45 minutes lobar liver ischemia and reperfusion. Tissue and blood samples were collected after 1h and 3h of reperfusion for histopathological study, plasma cytokines and alanine aminotransferase (ALT) measurement. RESULTS: The histopathological study demonstrated a significant reduction in liver necrosis in the RIPC group (p<0,001). The ALT levels were also significant lower in the RIPC group (p<0.01). The cytokines assessment showed that IL-6 levels were increased in the RIPC group after 1h of reperfusion, in comparison to the I/R group (p<0.05). Interleukin-10 levels in RIPC groups did not differ significantly from I/R group. CONCLUSIONS: Remote ischemic preconditioning is effective in decreasing liver necrosis in a rat model of ischemia-reperfusion. The IL-6 expression is up-regulated and peaked at 60 min of reperfusion. There was no difference in IL-10 expression between the groups. .

Vitis vinifera L. grape skin extract activates the insulin-signalling cascade and reduces hyperglycaemia in alloxan-induced diabetic mice.

OBJECTIVES: This study examined the effect of Vitis vinifera grape skin extract (ACH09) on hyperglycaemia and the insulin-signalling cascade in alloxan-treated mice. METHODS: Glycaemia, serum insulin and Western blot analysis of insulin cascade proteins were evaluated in the gastrocnemius muscles of four groups of adult mice: control, ACH09 (200 mg/kg per day, p.o.), alloxan (300 mg/kg, i.p.) and alloxan + ACH09. Insulin secretion in isolated pancreatic islets was also studied. KEY FINDINGS: Glycaemia values in the alloxan + ACH09 and ACH09 groups were significantly lower than in the alloxan-treated and control groups, respectively. Increased insulin resistance (HOMA index) was observed in the alloxan-treated group but not in the alloxan + ACH09 group. Insulin receptor content and Akt phosphorylation were significantly greater in the alloxan + ACH09 group compared with the alloxan-treated group. The glucose transporter (GLUT-4) content was reduced in alloxan-treated mice compared with the control group, while alloxan + ACH09 and ACH09-treated mice showed a significant increase in GLUT-4 content. ACH09 treatment did not change glucose-induced insulin secretion in isolated pancreatic islets. CONCLUSIONS: The results suggest that ACH09 has hypoglycaemic and antihyperglycaemic effects that are independent of an increase in insulin release but are probably dependent on an increase in insulin sensitivity resulting from an activation of the insulin-signalling cascade in skeletal muscle.

Appetite-related hormone levels in obese women with and without binge eating behavior / Hormônios reguladores do apetite em mulheres obesas com e sem compulsão alimentar

OBJECTIVE: The aim of this study was to evaluate serum levels of appetite-related hormones (peptide YY3-36, total ghrelin, leptin and insulin) before and after consumption of a meal in obese women with and without binge eating episodes and normal weight women. METHODS: Twenty-five women aged 32-50 years were invited to participate in this study, including 9 normal weight women without binge eating episodes (20-25kg/m², group 1), 9 obese women with binge eating episodes (³30kg/m², group 2), and 7 obese women without binge eating episodes (group 3). Four blood samples were collected from each participant, one being 60 minutes before and three being 15, 45 and 90 minutes after a meal. The composition of the meal was 55 percent carbohydrates, 15 percent protein and 30 percent lipids. RESULTS: Group 3 presented increased HOMA-IR (M=2.5, SD=1.04) when compared with group 1 (M=1.5, SD=0.53) and group 2 (M=1.8, SD=0.58), p=0.04. Body mass index (p<0.0001), leptin (p<0.0001) and insulin (p=0.01) were higher in group 3 than in the other groups before and after the meal. Additionally, total ghrelin (p=0.003) and PYY3-36 (p=0.02) levels were lower in group 2 than in the other groups before and after the meal. After adjustment for body mass index, only the lower PYY3-36 level of group 2 remained statistically different from the other groups (p=0.01). CONCLUSION: Our study suggests that lower levels of PYY 3-36 are associated with binge eating in obese women.

OBJETIVO: O objetivo deste estudo foi avaliar, antes e após a refeição, as concentrações séricas de hormônios ligados ao controle do apetite (peptídeo YY3-36, grelina total, leptina e insulina) em mulheres obesas com e sem episódios de compulsão alimentar e compará-las às mulheres de peso normal. MÉTODOS: Vinte e cinco mulheres com idade entre 32 e 50 anos foram convidadas a participar deste estudo, incluindo 9 mulheres com peso normal (20-25kg/m²) sem episódios de compulsão alimentar (grupo 1), 9 mulheres obesas (³30 kg/m²) com episódios de compulsão alimentar (grupo 2) e 7 mulheres obesas sem episódios de compulsão alimentar (grupo 3). Foram coletadas quatro amostras de sangue pós-prandiais a 60 minutos (1 hora antes), bem como 15, 45 e 90 minutos após uma refeição composta de 55 por cento de carboidratos, 15 por cento de proteínas e 30 por cento de lipídeos. RESULTADOS: O maior HOMA-IR foi observado no grupo 3 (M=2,5, DP=1,04) quando comparado ao grupo 1 (M=1,5, DP=0,53) e ao grupo 2 (M=1,8, DP=0,58), p=0,04. O índice de massa corporal (p<0,0001), a leptina (p<0,0001) e a insulina (p=0,01) foram maiores no grupo 3 antes e após a refeição. A grelina total (p=0,003) e o PYY3-36 (p=0,02) foram menores no grupo 2 antes e após a refeição. Após o ajuste do índice de massa corporal, apenas a baixa concentração de PYY3-36 no grupo 2 manteve-se estatisticamente diferente entre os grupos (p=0,01). CONCLUSÃO: Este estudo sugere que níveis baixos do PYY-3-36 estejam associados à compulsão alimentar em mulheres obesas.

Leptin/adiponectin ratio in obese women with and without binge eating disorder.

BACKGROUND: Adipose tissue-derived hormones are involved in the pathophysiology of eating disorders and other mental disorders. Studies have suggested that the serum leptin/adiponectin ratio is highly correlated with BMI. Furthermore, it is associated with a number of metabolic processes and inflammatory markers that are involved in obesity and mental disorders, such as the physiopathology of binge eating disorder (BED). We investigated whether variations in leptin and adiponectin serum concentrations differed between adult women with and without BED before and after a meal. METHODS: The study group was composed of 8 normal weight women (20-25 kg/m2) without BED, 8 obese women (>/=30 kg/m2) with BED, and 7 obese women without BED (non-BED). Blood samples were collected before and after the consumption of a meal composed of 55% carbohydrates, 15% protein, and 30% lipids. RESULTS: Body mass index (p<0.0001), leptin (p<0.0001) and the leptin/adiponectin ratio (p<0.0001) were higher in obese non-BED women than in obese BED and normal weight groups. Adiponectin (p=0.01) concentrations were lower in the obese BED group than in the other groups before and after the meal. CONCLUSIONS: The hypoadiponectinemia followed by the altered levels of leptin in obese BED woman may predispose these subjects to an inadequate energy balance, which could promote weight gain and an increased food intake in woman that may contribute to obesity and binge eating in these subjects.

Maternal protein restriction during early lactation induces GLUT4 translocation and mTOR/Akt activation in adipocytes of adult rats.

Epidemiological and experimental studies have demonstrated that early postnatal nutrition has been associated with long-term effects on glucose homeostasis in adulthood. Recently, our group demonstrated that undernutrition during early lactation affects the expression and activation of key proteins of the insulin signaling cascade in rat skeletal muscle during postnatal development. To elucidate the molecular mechanisms by which undernutrition during early life leads to changes in insulin sensitivity in peripheral tissues, we investigated the insulin signaling in adipose tissue. Adipocytes were isolated from epididymal fat pads of adult male rats that were the offspring of dams fed either a normal or a protein-free diet during the first 10 days of lactation. The cells were incubated with 100 nM insulin before the assays for immunoblotting analysis, 2-deoxyglucose uptake, immunocytochemistry for GLUT4, and/or actin filaments. Following insulin stimulation, adipocytes isolated from undernourished rats presented reduced tyrosine phosphorylation of IR and IRS-1 and increased basal phosphorylation of IRS-2, Akt, and mTOR compared with controls. Basal glucose uptake was increased in adipocytes from the undernourished group, and the treatment with LY294002 induced only a partial inhibition both in basal and in insulin-stimulated glucose uptake, suggesting an involvement of phosphoinositide 3-kinase activity. These alterations were accompanied by higher GLUT4 content in the plasma membrane and alterations in the actin cytoskeleton dynamics. These data suggest that early postnatal undernutrition impairs insulin sensitivity in adulthood by promoting changes in critical steps of insulin signaling in adipose tissue, which may contribute to permanent changes in glucose homeostasis.