8 research outputs found
Muscle wasting in cancer and ageing: Cachexia versus sarcopenia
No full textThe aim of this chapter is to summarize and evaluate the different mechanisms and catabolic mediators involved in cancer cachexia and ageing sarcopenia since they may represent targets for future promising clinical investigations. Cancer cachexia is a syndrome characterized by a marked weight loss, anorexia, asthenia and anemia. In fact, many patients who die with advanced cancer suffer from cachexia. The degree of cachexia is inversely correlated with the survival time of the patient and it always implies a poor prognosis. Unfortunately, at the clinical level, cachexia is not treated until the patient suffers from a considerable weight loss and wasting. At this point, the cachectic syndrome is almost irreversible. The cachectic state is often associated with the presence and growth of the tumour and leads to a malnutrition status due to the induction of anorexia. In recent years, age-related diseases and disabilities have become of major health interest and importance. This holds particularly for muscle wasting, also known as sarcopenia, that decreases the quality of life of the geriatric population, increasing morbidity and decreasing life expectancy. The cachectic factors (associated with both depletion of fat stores and muscular tissue) can be divided into two categories: of tumour origin and humoural factors. In conclusion, more research should be devoted to the understanding of muscle wasting mediators, both in cancer and ageing, in particular the identification of common mediators may prove as a good therapeutic strategies for both prevention and treatment of wasting both in disease and during healthy ageing
Formoterol and cancer muscle wasting in rats: Effects on muscle force and total physical activity
No full textMegestrol acetate: Its impact on muscle protein metabolism supports its use in cancer cachexia
No full textPunicic acid modulates mucosal immune responses and prevents gut inflammation through PPAR gamma and delta-dependent mechanisms
No full textCancer cachexia: Physical activity and muscle force in tumour-bearing rats
No full textRats bearing the Yoshida AH-130 ascites hepatoma are subjected to substantial weight loss, which is accompanied by anorexia at the end of the tumour cycle. Total physical activity (measured using the IR Actimeter system and Actitrack software) was determined during 11 days in control and tumour-bearing animals, skeletal muscle strength being also by the grip-strength test. The results presented clearly show that the presence of the tumour induces an earlier decrease in physical performance, which affects both skeletal muscle force and physical activity (both locomotor movements and stereotyped movements and distance travelled, among others parameters)
Catalpic acid decreases abdominal fat deposition, improves glucose homeostasis and upregulates PPAR a expression in adipose tissue
No full textBackground & aims: Catalpic acid (CAT) is a conjugated linolenic acid (CLN) isomer containing
trans-9, trans-11, cis-13 double bonds in an 18-carbon chain and it is found primarily in the
seed oil of ornamental and medicinal trees and shrubs of the family Bignoniaceae. The objective
of this study was to investigate whether CAT decreases obesity and ameliorates insulin
sensitivity and glucose tolerance in mice fed high-fat diets.
Methods: To test the efficacy of CAT in decreasing obesity and diabetes we used both a model
of diet-induced obesity (DIO) and a genetic model of obesity (i.e., mice lacking the leptin
receptor). Blood was collected on days 0, 7, 14, 21 and 28 for determining fasting glucose
and insulin concentrations in plasma. In addition, a glucose tolerance test was administered
on day 28.
Results: We found that dietary CAT (1 g/100 g) decreased fasting plasma glucose and insulin
concentrations, ameliorated the glucose normalizing ability following glucose challenge and
decreased abdominal white adipose tissue accumulation. In white adipose tissue (WAT), CAT
upregulated peroxisome proliferator-activated receptor (PPAR) a and its responsive genes
[i.e., stearoyl-coenzyme A desaturase (SCD1) and enoyl-coenzyme A hydratase (ECH)],
increased concentrations of high-density lipoprotein (HDL) cholesterol and decreased plasma
triglyceride (TG) levels
F4/80hiCCR2hi macrophage infiltration into the intra-abdominal fat worsens the severity of experimental IBD in obese mice with DSS colitis
No full textBackground & aims: Intra-abdominal fat is pathogenically involved in both type 2 diabetes and
inflammatory bowel disease (IBD). However, little is known about the interrelationships between these
two widespread and devastating diseases. The goal of this study is to investigate the effect of obesity in
the severity of colitis and, in turn, examine the impact of IBD on glucose tolerance during obesity. In this
context, we have explored the role of infiltrating macrophages in the severity of diabetes and IBD.
Methods: The infiltration of macrophages and T cells into intra-abdominal WAT, liver and the colonic
lamina propria was examined in db/db and lean mice after a 7-day dextran sodium sulfate (DSS) challenge
by tissue fractionation and flow cytometry. Disease activity indices (DAI), weight loss and colonic
histology were examined during the course of the DSS challenge, and colonic pro-inflammatory cytokine
expression was quantified by real-time RT-PCR. To determine the impact of obesity and intestinal
inflammation on glucose tolerance, mice were administered an intraperitoneal glucose tolerance test.
Results: We found that obesity increases the severity of experimental IBD. Following a DSS challenge,
obese mice express greater concentrations of colonic TNF-a mRNA than lean mice. In addition, experimental
IBD in combination with obesity worsens glucose tolerance beyond the effect caused by obesity
alone. F4/80hiCCR2hi macrophages infiltrate the lamina propria of mice with DSS colitis and the WAT of
obese mice.
Conclusions: Infiltration of F4/80hiCCR2hi macrophages into intra-abdominal fat worsens the severity of
experimental IBD during obesity. In turn, experimental IBD in obese mice repressed skeletal muscle PPAR
g and GLUT4 mRNA expression, upregulated MCP-1 and worsened type 2 diabetes
