scholarly journals Juice from leaves of cacti of the genus Pereskia: effect on the physiological parameters of Wistar rats

2020 ◽  
Vol 21 ◽  
Author(s):  
Débora Cristina Mariano Brasil ◽  
Rafaela Marchiori Mariano do Val ◽  
José Antônio de Souza Cruz Ramos ◽  
Martha Elisa Ferreira de Almeida

Abstract The objective was to evaluate whether the juice from the leaves of cacti of three species of the genus Pereskia promotes changes in the physiological parameters of Wistar rats. The study was divided into stage 1 (obesity induction with a hypercaloric diet, monosodium glutamate, and sucrose solution), and stage 2 (use of cactus juice). The data of body weight, Body Mass and Lee Indexes, feed intake, adipose tissue mass, and Visceral and Epididymal Fat Indexes were compared by the Tukey test at 5%. Monosodium glutamate and sucrose in association with the hypercaloric diet did not increase adipose tissues. No statistical difference was found between the means of body weight, Body Mass Index and Lee Index, liver weight, and Hepatosomatic Index. Pereskia grandifolia juice promoted a lower total weight gain due to the low feed intake. Pereskia aculeata juice increased the visceral adipose tissue mass. Thus, the Pereskia grandifolia juice presented a better effect on weight gain. These cacti are rich in nutrients and bioactive compounds that can improve food quality, and prevent chronic non-communicable diseases.

2019 ◽  
Author(s):  
Lidewij Schipper ◽  
Steffen van Heijningen ◽  
Giorgio Karapetsas ◽  
Eline M. van der Beek ◽  
Gertjan van Dijk

AbstractIndividual housing from weaning onwards resulted in reduced growth rate during adolescence in male C57Bl/6J mice that were housed individually, while energy intake and energy expenditure were increased compared to socially housed counterparts. At 6 weeks of age, these mice had reduced lean body mass, but significantly higher white adipose tissue mass compared to socially housed mice. Body weight gain of individually housed animals exceeded that of socially housed mice during adulthood, with elevations in both energy intake and expenditure. At 18 weeks of age, individually housed mice showed higher adiposity and higher mRNA expression of UCP-1 in inguinal white adipose tissue. Exposure to an obesogenic diet starting at 6 weeks of age further amplified body weight gain and adipose tissue deposition. This study shows that post-weaning individual housing of male mice results in impaired adolescent growth and higher susceptibility to obesity in adulthood. Mice are widely used to study obesity and cardiometabolic comorbidities. For (metabolic) research models using mice, (social) housing practices should be carefully considered and regarded as a potential confounder due to their modulating effect on metabolic health outcomes.


2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Yang Sam Jung ◽  
Pei Chin Tsung ◽  
Byoung Chul Kim ◽  
Jong Hoon Kim ◽  
Hoa Jun Seok ◽  
...  

2014 ◽  
Vol 393 (1-2) ◽  
pp. 120-128 ◽  
Author(s):  
M. Holubová ◽  
V. Nagelová ◽  
Z. Lacinová ◽  
M. Haluzík ◽  
D. Sýkora ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
H. Roger Lijnen ◽  
Kathleen Freson ◽  
Marc F. Hoylaerts

Background. The pituitary adenylate cyclase activating polypeptide (PACAP) may affect adipogenesis and adipose tissue formation through interaction with its G-protein-coupled receptor VPAC1.Methods. We have used a monoclonal antibody (MAb 23A11) blocking VPAC1 in mouse models of nutritionally induced obesity.Results. Administration of MAb 23A11 (25 mg/kg body weight i.p. twice weekly) to 5-week old male C57Bl/6 mice kept on a high-fat diet for 15 weeks had no significant effect on weight gain, nor on subcutaneous (SC) or gonadal (GON) adipose tissue mass, as compared to the control MAb 1C8. However, adipocyte hypertrophy was observed in SC adipose tissue of MAb 23A11 treated mice. In a second study, 24 weeks old obese mice were treated for 5 weeks with MAb 23A11, without effect on body weight or fat mass, as compared to treatment with MAb 1C8. In addition, MAb 23A11 had no significant effect on glucose tolerance or insulin resistance in lean or obese C57Bl/6 mice.Conclusion. Blocking VPAC1 does not significantly affect adipose tissue formation in mouse models of diet-induced obesity, although it may be associated with mild adipocyte hypertrophy.


1997 ◽  
Vol 93 (4) ◽  
pp. 349-354 ◽  
Author(s):  
Jacopo P. Mortola ◽  
Lina Naso

1. Hypoxia is known to decrease thermogenesis. We set out to determine whether this is accompanied by alterations in the brown adipose tissue, which is a major source of non-shivering thermogenesis. 2. Measurements were performed on 25- and 64-day-old rats, after 4 days of hypoxia (10% inspired O2), and on ∼3.5-month-old rats in hypobaric hypoxia since birth, at an ambient temperature of 25°C. 3. All hypoxic rats had higher haematocrit and lower body mass than corresponding controls. 4. In the 25-day-old rats, hypoxia had minimal and non significant effects on brown adipose tissue mass, proteins and DNA concentration. The content of the mitochondrial uncoupling protein thermogenin, evaluated by immunoblot after electrophoretic separation, relative to the cytoskeleton actin (UCP/Act), was not significantly altered. 5. In 25-day-old rats exposed for 4 days to cold (ambient temperature = 7–9°C), brown adipose tissue was hyperplastic, with increased UCP/Act; hypoxia did not appreciably alter the response to cold. 6. In the 2-month-old rats, after 4 days of hypoxia UCP/Act was reduced to about 40% of control. 7. In the 3.5-month-old rats maintained in hypoxia since birth, brown adipose tissue mass was reduced in proportion to body mass, with little effect on total proteins and DNA; UCP/Act was decreased to about 50% of control. 8. We conclude that chronic hypoxia had a minimal effect on brown adipose tissue total proteins and DNA content. However, the uncoupling protein content can be greatly reduced, depending upon age and duration of hypoxia.


2020 ◽  
Author(s):  
Qingmin Zeng ◽  
Lili Zhao ◽  
Chao Meng ◽  
Xiaotong Zhao ◽  
Yonggang Liu ◽  
...  

Abstract Background: Epidemiological studies support the association between inadequate vitamin C (Vc) intake and non-alcoholic fatty liver disease (NAFLD). However, the intervention dose of Vc and the mechanisms of its action in NAFLD are unclear. This study aimed to investigate the prophylactic and therapeutic effects of low, medium and high doses of Vc on NAFLD. Methods: C57BL/6 mice were randomly assigned to prophylactic groups or therapeutic groups. Each group had five subgroups: control subgroup (C), high-fat subgroup (HF), low-dose Vc subgroup (15 mg/kg per day, LVc), medium-dose Vc subgroup (30 mg/kg per day, MVc), and high-dose Vc subgroup (90 mg/kg per day, HVc). In prophylactic groups, mice received high-fat diet (HFD) and simultaneously supplied with different doses Vc for 12 weeks. In therapeutic groups, mice were fed HFD for 6 weeks to form NAFLD model, and then treated with different dose Vc for 12 weeks. Results: Prophylactic LVc and MVc administration reduced the risk of NAFLD development in HFD-fed mice, as evidenced by significantly lowered body weight, perirenal adipose tissue mass, and steatosis, whereas prophylactic HVc administration did not prevent HFD-induced NAFLD development. Furthermore, therapeutic MVc administration significantly ameliorated HFD-induced increase in body weight, perirenal adipose tissue mass and steatosis, whereas therapeutic LVc and HVc administration did not ameliorate NAFLD symptoms. In fact, therapeutic HVc administration significantly increased body weight, perirenal adipose tissue mass and lobular inflammation. Moreover, prophylactic LVc administration was more effective than therapeutic LVc administration as evidenced by significantly lower body weight, perirenal adipose tissue mass, steatosis, ballooned hepatocytes, and lobular inflammation in the prophylactic LVc subgroup. And same trends were observed between prophylactic HVc administration and therapeutic HVc administration. In addition, all Vc-administered mice exhibited low blood glucose, triglycerides, and homeostasis model assessment of insulin resistance values and high adiponectin levels compared to HF mice. Conclusion: MVc was beneficial for HFD-induced NAFLD prophylaxis and therapy. LVc prevented HFD-induced NAFLD development, while HVc for NAFLD management was risky. This study offers valuable insight into the effect of various Vc doses on NAFLD management.


1999 ◽  
Vol 79 (2) ◽  
pp. 451-480 ◽  
Author(s):  
Eric Jéquier ◽  
Luc Tappy

The mechanisms involved in body weight regulation in humans include genetic, physiological, and behavioral factors. Stability of body weight and body composition requires that energy intake matches energy expenditure and that nutrient balance is achieved. Human obesity is usually associated with high rates of energy expenditure. In adult individuals, protein and carbohydrate stores vary relatively little, whereas adipose tissue mass may change markedly. A feedback regulatory loop with three distinct steps has been recently identified in rodents: 1) a sensor that monitors the size of adipose tissue mass is represented by the amount of leptin synthesized by adipose cells (a protein encoded by the ob gene) which determines the plasma leptin levels; 2) hypothalamic centers, with specific leptin receptors, which receive and integrate the intensity of the signal; and 3) effector systems that influence the two determinants of energy balance, i.e., energy intake and energy expenditure. With the exception of a few very rare cases, the majority of obese human subjects have high plasma leptin levels that are related to the size of their adipose tissue mass. However, the expected regulatory responses (reduction in food intake and increase in energy expenditure) are not observed in obese individuals. Thus obese humans are resistant to the effect of endogenous leptin, despite unaltered hypothalamic leptin receptors. Whether defects in the leptin signaling cascade play a role in the development of human obesity is a field of great actual interest that needs further research. Present evidences suggest that genetic and environmental factors influence eating behavior of people prone to obesity and that diets that are high in fat or energy dense undermine body weight regulation by promoting an overconsumption of energy relative to need.


2020 ◽  
Vol 40 (3) ◽  
pp. 170-175
Author(s):  
Rodrigo M. Ribeiro ◽  
Debora S.F. Ribeiro ◽  
Cahue F.R. Paz ◽  
Alexandre A.O. Gobesso ◽  
Rafael R. Faleiros

ABSTRACT: In recent years, several researchers have been studying obesity in national horse breeds; however, no studies demonstrating the dynamic of body and regional fat accumulation (adiposity) Mangalarga Marchador horses subjected to hypercaloric diets have been found. This study aimed to characterize the deposition of body and regional fat in horses with diet-induced weight gain. A total of nine Mangalarga Marchador adult horses with initial body condition score (BCS) of 2.9 ±1/9 (mean ±SD) were subjected to a hypercaloric, grain-rich diet for five months. Body weight and the following morphometric regional adiposity variables were analyzed: BCS, cresty neck scores (CNS), neck circumferences (NC) at 25, 50 and 75% of its length, and accumulation of subcutaneous adipose tissue at the base of the tail using ultrasonography (BTU). These data were collected at baseline and fortnightly after beginning the diet-induced weight gain until the end of the experiment. The effect of time on the variables was verified by analysis of variance (ANOVA) in randomized blocks or the Friedman’s test, and the means were compared by the Tukey’s test (p≤0.05). Exposure to hypercaloric diet promoted a mean weight gain of 27.45% (p<0.001). Significant values were observed for NC at 25 and 75% during the first 45 days of the experiment, and for NC at 50% during the first 30 days. BTU presented significant changes after 60 days, with an increase of 268% compared with the baseline value. These findings demonstrate the weight gain and the dynamic and magnitude of regional adiposity in Mangalarga Marchador horses subjected to hypercaloric diet.


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