Juçara pulp supplementation improves glucose tolerance in mice.

BACKGROUND: The consumption of hyperlipidic and hypercaloric diet is considered a major factor to promote obesity and the consumption of food with antioxidant properties, like Juçara (Euterpe edulis Mart), could be a tool to prevent the deleterious effect of high white adipose deposition. The aim of the present study was to evaluate the effect of administration of juçara pulp in mice fed a high-fat, high-calorie diet on glucose tolerance and adipose tissue inflammatory status. METHODS: Mice were distributed into the following groups: control diet; control diet plus 0.5 % of juçara; control diet plus 2 % of juçara; hypercaloric and hyperlipidic diet; hypercaloric and hyperlipidic diet plus 0.5 % of juçara and hypercaloric and hyperlipidic diet plus 2 % of juçara. Treatments started when mice were 8 weeks old and carried on for a total period of 10 weeks. The serum glucose, triacylglycerol, total cholesterol, insulin, adiponectin, lipopolysaccharides and free fatty acids concentrations were measured. Oral glucose tolerance test was performed. TNF-α, IL-6, and IL-10 protein level were determined by ELISA on mesenteric and epididymal white adipose tissues. Determination of catalase activity was realized in the same tissues. Data were analysed using one-way analysis of variance and post hoc analysis was performed with the Tukey's test. RESULTS: The addition of 0.5 % juçara improved glycemic response in animals that consumed normocaloric as well as hypercaloric and hyperlipidic diets (HC). Supplementation with 0.5 and 2 % did not change the body composition of animals that received the HC diet; however, the animals fed the normocaloric diet with 2 % juçara gained body mass. An intake of 2 % juçara in the HC diet promoted a reduction of catalase activity and IL-10 level in epididymal adipose tissue. CONCLUSIONS: These results suggest that with the administration of 0.5 % juçara, the beneficial effects of polyphenols overcome the deleterious effects of macronutrient composition of juçara, whereas with the administration of 2 % juçara promotes damage by the composition of the fruit and overshadows the beneficial effects of polyphenols on glucose metabolism. On the other hand, higher juçara supplementation improves the inflammatory status targeted by the HC diet.

Reduction in saturated fat intake improves cardiovascular risks in obese adolescents during interdisciplinary therapy.

BACKGROUND/OBJECTIVES: Obesity is related to inflammation and cardiovascular disease. The increase in saturated fatty acid intake (SFA) can potentiate cardiovascular risks. The aim of this study was to assess the influence of change in SFA on carotid intima-media thickness (cIMT), metabolic profile and anti/pro-inflammatory adipokines in obese adolescents. METHODS: Sixty obese adolescents were subjected to 1 year of interdisciplinary intervention (nutrition, psychology, physical exercise and clinical therapy). Blood glucose, insulin, lipid profile, leptin and adiponectin were analysed. Insulin resistance was estimated by HOMA-IR and HOMA-AD. cIMT was measured by ultrasonography. Dietetic intake was calculated by 3-day dietary record. Volunteers were analysed according to tertiles of change (Δ) in SFA intake: Low-SFA reduction<3.68 g; Moderate-SFA reduction 3.68-13.67 g; and High-SFA reduction>13.67 g. RESULTS: Moderate and High-SFA tertiles presented reduction in insulin, leptin/adiponectin ratio, cIMT and increase in adiponectin and adiponectin/leptin ratio. Adiponectin/leptin ratio was predictor of cIMT. HOMA-IR, total cholesterol and LDL-cholesterol reduced only in High-SFA tertile, and was associated with SFA independent of visceral fat. Negative correlations between Δ of SFA and adiponectin and adiponectin/leptin ratio were observed. CONCLUSION: Obese adolescents with moderate and high reduction in SFA presented improvements on pro/anti-inflammatory biomarkers and cIMT, leading to reduction in cardiovascular risks.

Chronic exercise promotes alterations in the neuroendocrine profile of elderly people.

Aging and physical inactivity are 2 factors that favour the development of cardiovascular disease, metabolic syndrome, obesity, and diabetes. In contrast, adopting a habitual moderate exercise routine may be a nonpharmacological treatment alternative for neuroendocrine aging disorders. We aimed to assess the effects of moderate exercise training on the metabolic profiles of elderly people with sedentary lifestyles. Fourteen sedentary, healthy, elderly male volunteers participated in a moderate training regimen for 60 min/day, 3 days/week for 24 weeks at a work rate equivalent to their ventilatory aerobic threshold. The environment was maintained at a temperature of 23±2°C, with a humidity of 60±5%. Blood samples for analysis were collected at 3 intervals: at baseline (1 week before training began), and 3 and 6 months after training. The training promoted increased aerobic capacity (relative VO(2), and time and velocity to VO(2)max; (p<0.05)) and reduced serum α-MSH (p<0.05) after 3 months of training when compared with the baseline data. In addition, serum thyroid hormone (T3 and T4) was reduced after 6 months of training compared with baseline levels. Our results demonstrate that a moderate exercise training protocol improves the metabolic profile of older people, and metabolic adaptation is dependent on time.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 µg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration.

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 microg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables.

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17% protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6%). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17 percent protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6 percent). Independent of the protein content of the diet, pregnancy increased total (F1,19 = 22.28, P < 0.001) and relative (F1,19 = 5.57, P < 0.03) food intake, the variation of weight (F1,19 = 49.79, P < 0.000) and final body weight (F1,19 = 19.52, P < 0.001), but glycemia (F1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F1,19 = 18.13, P < 0.001) and low-protein diet (F1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

Lipid metabolism of monosodium glutamate obese rats after partial removal of adipose tissue.

We analyzed the effects of partial fat pad removal on retroperitoneal and epididymal fat depots and carcass metabolism of control (C) and MSG-obese (M) rats. Three-month-old C and M male Wistar rats were submitted to either partial surgical excision of epididymal and retroperitoneal fat tissue (lipectomy, L) or sham surgery (S) and studied after 7 or 30 days. Retroperitoneal and epididymal tissue re-growth after lipectomy was not observed, as indicated by the low pads weight of the L groups. The lipolysis rate was stimulated in LC7 and LM7, probably due to surgical stress and low insulin levels. In LM7, but not in LC7, in vivo lipogenesis rate increased in retroperitoneal and epididymal fat tissue, as did the diet-derived lipid accumulation in epididymal fat tissue. Although these local increases were no longer present in LM30, this group showed a large increase in the percentage of small area adipocytes in both pads as well as increased carcass lipogenesis rate. The present data showed that the partial removal of fat depots affected the metabolism of control and MSG-obese rats differently. In the obese animals only, it stimulated both local and carcass lipogenesis rate as well as adipocyte differentiation, i.e. responses likely to favor excised tissue re-growth and/or compensatory growth of non-excised depots.

Effect of ethanol intake during lactation on male and female pups' liver and brain metabolism during the suckling-weaning transition period.

In rats, a high degree of brain development and myelination occurs during the first 15 days after birth. Ethanol intake by lactating rats modified 12 day-old pups' brain development and metabolism. The aim of the present study was to evaluate the effect of maternal ethanol ingestion during lactation on prepubertal (24-day-old) pups' brain and liver metabolism. Lactating rats (4 male and 4 female litters) were divided into 2 groups: control--received control liquid diet, and ethanol--received liquid diet containing 4% of ethanol. On postnatal day 24, the pups were killed by decapitation. Liver and brain were utilized for measuring Adenosine Tri-phosphate-citrate lyase and malic enzymes activities. Brain slices were incubated in medium containing glucose to determine glucose consumption and oxidation, and lipid synthesis. The ethanol intake decreased male and female pups' body, brain and liver weight. Liver Adenosine Tri-phosphate-citrate lyase activity was decreased only in male pups of the ethanol group. The intake of ethanol solution by the dams increased glucose consumption and oxidation by the incubated female pups' brain slices and decreased glucose oxidation by the male pups' brain slices. It can be concluded that the effects of maternal ethanol intake on pups' development and metabolism are gender-related.

Ethanol intake during lactation. I. Effects On dams' metabolism and pups' body weight gain.

Wistar lactating rats (8 pups per dam) had free access to either tap water (control group, C) or one of three concentrations of ethanol (E) in the drinking water: 5% (E5), 10% (E10), and 20% (E20). All animals received normal rat chow ad libitum and were killed on day 12 of lactation. Intake of both 10% and 20% ethanol solutions decreased food intake, dams' body weight, and pups' body weight gain as compared with findings in the C group. The relative weights (g/100g b.w.) of the mammary glands (MG) and of the parametrial white adipose tissue depot were decreased only in E20 as compared with findings in the C group. Protein and lipid content of these tissues were not altered in any of the ethanol groups. In comparison with the C group, the lipogenesis rate was increased in the MG (135. 6%) and liver (120.2%) in E5 and the MG (58.1%) and parametrial white adipose tissue depot (147.0%) in E20. No modifications in lipogenesis rate were noted in E10. The malic enzyme activity was decreased in the MG in E10 (25.3%) and E20 (26.4%) and in the liver in E20 (45.7%). In E5, however, it was increased in the liver (23. 9%). The activity of ATP-citrate lyase in the liver was decreased in E20 (56.7%), while it was increased by 37.5% in E5 and 34.2% in E10. Blood glucose concentration of dams was not affected by ethanol ingestion. However, plasma triacylglycerol concentration was higher in E10 (17.9%) and E20 (13.3%) than in the C group, and plasma protein was lower in E20 (15.7%) than in C. We concluded that alcohol intake during lactation increased the MG lipogenesis rate; although at the highest dose, this metabolic alteration was not enough to allow normal pups' growth. However, the low dose of ethanol (5%), despite having altered dams' metabolism, did not affect pups' body weight gain.

Ethanol intake during lactation. II. Effects On pups' liver and brain metabolism.

Lactating rats, with litters adjusted to 8 pups on day 1, were divided into 4 groups: control animals (C), which received water and Nuvilab chow ad libitum, and ethanol animals (E), which received 20% (E20), 10% (E10), or 5% (E5) ethanol diluted in the drinking water and Nuvilab chow ad libitum. On day 12 of life, the pups were weighed and decapitated. The intake of 10% and 20% ethanol solutions by the lactating rats decreased the pups' body weight and liver weight. The pups' liver ATP-citrate lyase activity was decreased in all ethanol groups. The pups' brain weight decreased in E20 only. Glucose metabolism and lactate production were studied in the pups' brain slices, which were incubated at 37 degrees C in Krebs-Henseleit buffer under carbogen in the presence of glucose (5 mM) plus 14C-glucose (0.04 microCi) with or without beta-hydroxybutyrate or insulin. Study of the incubated pups' brain slices showed that the intake of the 20% ethanol solution by the dams increased glucose consumption, oxidation, lactate production, and lipogenesis rate from glucose in all media studied, as compared with findings in the C group. In the pups' brain slices, the lactate production and lipogenesis rate from glucose were higher in E10 than in the C group. The addition of beta-hydroxybutyrate to the incubation medium caused a decrease in glucose oxidation in C, E5, and E20 and an increase in glucose consumption in E10. Ingestion of the 5% ethanol solution by dams decreased the pups' brain lipogenesis rate from glucose in all media studied. We concluded that the effects of maternal alcohol intake on the pups' development and metabolism are dose-dependent. High amounts of ethanol intake (10% or 20%) caused a great impairment in the pups' growth, as well as their liver and brain metabolism. The low dose (5%) did not affect the pups' body weight gain or their brain and liver weight, but it did alter brain glucose metabolism.

Ethanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of beta-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.

Re-examination of the putative roles of insulin and prolactin in the regulation of lipid deposition and lipogenesis in vivo in mammary gland and white and brown adipose tissue of lactating rats and litter-removed rats.

1. The effects of various treatments to alter either plasma prolactin (bromocryptine administration or removal of litter) or the metabolic activity of the mammary gland (unilateral or complete teat sealing) on the disposal of oral [14C]lipid between 14CO2 production and [14C]lipid accumulation in tissues of lactating rats were studied. In addition, the rates of lipogenesis in vivo were measured in mammary gland, brown and white adipose tissue and liver. 2. Bromocryptine administration lowered plasma prolactin, but did not alter [14C]lipid accumulation in mammary gland or in white and brown adipose tissue. 3. In contrast, complete sealing of teats results in no change in plasma prolactin, but a 90% decrease in [14C]lipid accumulation in mammary gland and a 4-fold increase in white and brown adipose tissue. The rate of lipogenesis in mammary gland was decreased by 95%, but there was no change in the rate in white and brown adipose tissue. Unilateral sealing of teats resulted in a decrease in [14C]lipid accumulation in white adipose tissue. 4. Removal of the litter for 24 h (low prolactin) produced a similar pattern to complete teat sealing, except that there was a 6-fold increase in lipogenesis in white adipose tissue. Re-suckling for 5 h increased plasma prolactin, but did not alter the response seen in litter-removed lactating rats. 5. Changes in lipoprotein lipase activity and in plasma insulin paralleled the reciprocal changes in [14C]lipid accumulation in white and brown adipose tissue and in mammary gland. 6. It is concluded that the plasma insulin is more important than prolactin in regulating lipid deposition in adipose tissue during lactation, and that any effects of prolactin must be indirect.

Tissue-specific effects of starvation and refeeding on the disposal of oral [1-14C]triolein in the rat during lactation and on removal of litter.

1. The effects of starvation and refeeding on the disposal of oral [14C]triolein between 14CO2 production and 14C-lipid accumulation in tissues of virgin rats, lactating rats and lactating rats with pups removed were studied. 2. Starvation (24 h) increased 14CO2 production in lactating rats and lactating rats with pups removed to values found in virgin rats. This increase was accompanied by decreases in 14C-lipid accumulation in mammary gland and pups of lactating rats and in white and brown adipose tissue of lactating rats with pups removed. 3. Short-term (2 h) refeeding ad libitum decreased 14CO2 production in lactating rats and lactating rats with pups removed, and restored the 14C-lipid accumulation in mammary glands plus pups and in white and brown adipose tissue respectively 4. Insulin deficiency induced with mannoheptulose inhibited the restoration of 14C-lipid accumulation in white adipose tissue on refeeding of lactating rats with pups removed, but did not prevent the restoration of 14C-lipid accumulation in mammary gland. 5. Changes in the activity of lipoprotein lipase in mammary gland and white adipose tissue paralleled the changes in 14C-lipid accumulation in these tissues. 6. It is concluded that 14C-lipid accumulation in mammary gland may not be affected by changes in plasma insulin concentration and that it is less sensitive to starvation than is lipogenesis or lactose synthesis. This has the advantage that the milk lipid content can still be maintained from hepatic very-low-density lipoprotein for a period after withdrawal of food. The major determinant of the disposal of oral 14C-triolein appears to be the total tissue activity of lipoprotein lipase. When this is high in mammary gland (fed lactating rats) or white adipose tissue (fed lactating rats with pups removed), less triacylglycerol is available for the muscle mass and consequently less is oxidized.

Time course of insulin, corticosterone and metabolic changes caused by lesion of the ventromedial hypothalamus in the rat.

The time course of changes in glycemia, insulinemia, corticosteronemia, liver glycogen, food intake, body and stomach's fresh weight were studied in rats subjected to electrolytic bilateral destruction of the ventromedial hypothalamus (VMH) and in a sham-operated (SO) group. Some of these parameters were determined during the first four hours after lesioning and all were measured also up to two weeks. Glycemia increased steadily, attaining 37.1% 120 min post-lesioning, and a parallel decrease (51.3%) in hepatic glycogen was observed. Twenty minutes after VMH destruction the insulin levels were 215.8% higher than in the SO group, a difference that was reversed 220 min later. At the first day post-lesioning the insulin levels increased 348%. It is suggested that the release was stimulated by the early reflex insulin secretion elicited by food ingestion. During the first hours after VMH lesioning corticosteronemia was elevated to 253.9% of the corresponding parameter in the SO group. When the effects of the lesion were followed up during fifteen days it was found that glycemia and hepatic glycogen returned to normal levels but insulinemia went up again. Plasma insulin increased 325.9% by the end of the observation period while corticosteronemia was 404.5% higher as compared with the SO animals. Food intake increased 63.5% on the day after lesioning and continued to rise, attaining 106% by the fifteenth day, which paralleled the weight gain (31%). A close topographic correlation was found in this study between the precise lesioning of the ventromedial nuclei of the hypothalamus and the changes herein described.

Evidence for conservation of dietary lipid in the rat during lactation and the immediate period after removal of the litter. Decreased oxidation of oral [1-14C]triolein.

Production of 14CO2 from an oral load of [1-14C]triolein was greatly decreased (70%) in lactating rats or immediately after (24-48 h) removal of the litter, compared with virgin rats. This decreased oxidation of dietary lipid was accompanied by accumulation of 14C-labelled lipid in lactating mammary gland or adipose tissue (after litter removal). No difference in 14CO2 production between lactating and virgin rats was observed when [1-14C]octanoate was administered. It is concluded that a major factor in this conservation of dietary triacylglycerol is the relative activity of lipoprotein lipase in the tissues.