Loss Of Tissue Mass Research Articles

Use of higher-protein diets during intense military training to decrease lean tissue loss and improve performance

Background Current dietary intakes of active military personnel during intense training sessions may result in loss of lean tissue mass due to lower intake of energy and protein. It was hypothesized that a higher-protein diet (HPD) with frequent meals would result in greater lean tissue maintenance and improved performance during intense military training. Design 36 Air Force cadets completed a 12-day training session. A HPD (40% carbohydrate, 30% protein, 30% fat) with frequent meals was prescribed to each participant. Cadets completed 4 hours of supervised exercise daily. Pre- and post-test assessments included: body weight, body composition, vertical jump height, leg power index (LPI) and anaerobic testing. Results A negative correlation was found between the change in average vertical jump height and protein intake. Total body mass increased by 0.6 ± 1.1 kg (p<.001), and percent body fat decreased by 1.1 ± 0.9 (p<.001). Fat-free mass increased by 1.3 ± 1.1 kg (p<.001), fat-mass decreased by 0.7 ± 0.7 (p<.001). Averaged 600 meter times decreased by 1.2 ± 1.8 seconds (p<.001). Peak LPI (LPI) and average LPI increased by 0.12 ± 0.22 (p<.001) and 0.13 ± 0.22 (p<.001), respectively. Total energy intake was 14,110 ± 4,389 kJ. Macronutrient breakdown of diets was 52 ± 11% carbohydrates (437 ± 155 g), 19 ± 4% protein (157 ± 65 g) and 32 ± 9% fat (119 ± 53 g). There was no correlation between meal frequency and anthropometric changes or performance changes. Meal frequency consisted of 64% of the subjects consuming 3 meals and 1 to 3 snacks daily, 22% of the subjects only consumed 2 meals and 1 to 3 snacks daily, and 13% of participants reported consuming 2 large meals and no snacks daily. Conclusion Frequent meals and snacking appears to have resulted in maintenance and an increase in fat-free mass. The increase in LPI may be partially due to the increase in FFM. However, due to lack of dietary adherence, the hypothesis of this study could not be tested accurately.

C9t11‐Conjugated linoleic acid‐rich oil fails to attenuate wasting in colon‐26 tumor‐induced late‐stage cancer cachexia in male CD2F1 mice

Cancer cachexia is characterized by muscle and adipose tissue wasting caused partly by chronic, systemic inflammation. Conjugated linoleic acids (CLAs) are a group of fatty acids with various properties including anti-inflammatory cis9, trans11 (c9t11)-CLA and lipid-mobilizing trans10, cis12 (t10c12)-CLA. The purpose of this study was to test whether dietary supplementation of a c9t11-CLA-rich oil (6:1 c9t11:t10c12) could attenuate wasting of muscle and adipose tissue in colon-26 adenocarcinoma-induced cachexia in mice. Loss of body weight, muscle and adipose tissue mass caused by tumors were not rescued by supplementation with the c9t11-CLA-rich oil. In quadriceps muscle, c9t11-CLA-rich oil exacerbated tumor-induced gene expression of inflammatory markers tumor necrosis factor-α, IL-6 receptor and the E3 ligase MuRF-1 involved in muscle proteolysis. In epididymal adipose tissue, tumor-driven delipidation and atrophy was aggravated by the c9,t11-CLA-rich oil, demonstrated by further reduced adipocyte size and lower adiponectin expression. However, expression of inflammatory cytokines and macrophage markers were not altered by tumors, or CLA supplementation. These data suggest that addition of c9t11-CLA-rich oil (0.6% c9t11, 0.1% t10c12) in diet did not ameliorate wasting in mice with cancer cachexia. Instead, it increased expression of inflammatory markers in the muscle and increased adipose delipidation.

Selective deletion of adipocytes, but not preadipocytes, by TNF-α through C/EBP- and PPARγ-mediated suppression of NF-κB

Tumor necrosis factor-α (TNF-α) is a key regulator of adipose tissue mass, but mechanisms underlying this effect have not been fully elucidated. We found that exposure to TNF-α caused a significant decrease in the number of adipocytes, but not preadipocytes. Subsequent experiments revealed that TNF-α selectively deleted adipocytes through induction of apoptosis. Following exposure to TNF-α, rapid activation of nuclear factor-κB (NF-κB) was observed only in preadipocytes, but not in adipocytes. Inhibition of NF-κB rendered preadipocytes susceptible to TNF-α-induced apoptosis, suggesting that different activity of NF-κB is the determinant for the distinct apoptotic responses. During adipocyte differentiation, expression and activity of peroxisome proliferator-activated receptor-γ (PPARγ) were upregulated. Treatment of preadipocytes with a PPARγ agonist attenuated NF-κB activation and rendered the cells vulnerable to TNF-α-induced apoptosis. Conversely, treatment of adipocytes with a PPARγ antagonist enhanced NF-κB activation and conferred resistance to TNF-α-induced apoptosis, suggesting involvement of PPARγ in the suppression of NF-κB in adipocytes. We also found that, following differentiation, expression and activity of CCAAT/enhancer binding protein (C/EBP), especially C/EBPα and C/EBPβ, were upregulated in adipocytes. Overexpression of individual C/EBPs significantly inhibited activation of NF-κB in preadipocytes. Furthermore, transfection with siRNA for C/EBPα or C/EBPβ enhanced activity of NF-κB in adipocytes, suggesting that C/EBP is also involved in the repression of NF-κB in adipocytes. These results suggested novel mechanisms by which TNF-α selectively deletes adipocytes in the adipose tissue. The C/EBP- and PPARγ-mediated suppression of NF-κB may contribute to TNF-α-related loss of adipose tissue mass under certain pathological situations, such as cachexia.

Additive actions of the cannabinoid and neuropeptide Y systems on adiposity and lipid oxidation

Energy homeostasis is regulated by a complex interaction of molecules and pathways, and new antiobesity treatments are likely to require multiple pharmacological targeting of anorexigenic or orexigenic pathways to achieve effective loss of excess body weight and adiposity. Cannabinoids, acting via the cannabinoid-1 (CB1) receptor, and neuropeptide Y (NPY) are important modulators of feeding behaviour, energy metabolism and body composition. We investigated the interaction of CB1 and NPY in the regulation of energy homeostasis, hypothesizing that dual blockade of CB1 and NPY signalling will induce greater weight and/or fat loss than that induced by single blockade of either system alone. We studied the effects of the CB1 antagonist Rimonabant on food intake, body weight, body composition, energy metabolism and bone physiology in wild-type (WT) and NPY knockout (NPY(-/-)) mice. Rimonabant was administered orally at 10 mg/kg body weight twice per day for 3 weeks. Oral Rimonabant was delivered voluntarily to mice via a novel method enabling studies to be carried out in the absence of gavage-induced stress. Mice with dual blockade of CB1 and NPY signalling (Rimonabant-treated NPY(-/-) mice) exhibited greater reductions in body weight and adiposity than mice with single blockade of either system alone (Rimonabant-treated WT or vehicle-treated NPY(-/-) mice). These changes occurred without loss of lean tissue mass or bone mass. Furthermore, Rimonabant-treated NPY(-/-) mice showed a lower respiratory exchange ratio than that seen in Rimonabant-treated WT or vehicle-treated NPY(-/-) mice, suggesting that this additive effect of dual blockade of CB1 and NPY involves promotion of lipid oxidation. On the other hand, energy expenditure and physical activity were comparable amongst all treatment groups. Interestingly, Rimonabant similarly and transiently reduced spontaneous and fasting-induced food intake in WT and NPY(-/-) mice in the first hour after administration only, suggesting independent regulation of feeding by CB1 and NPY signalling. In contrast, Rimonabant increased serum corticosterone levels in WT mice, but this effect was not seen in NPY(-/-) mice, indicating that NPY signalling may be required for effects of CB1 on the hypothalamo-pituitary-adrenal axis. Dual blockade of CB1 and NPY signalling leads to additive reductions in body weight and adiposity without concomitant loss of lean body mass or bone mass. An additive increase in lipid oxidation in dual CB1 and NPY blockade may contribute to the effect on adiposity. These findings open new avenues for more effective treatment of obesity via dual pharmacological manipulations of the CB1 and NPY systems.

Treadmill Exercise And IL-6-induced Cachexia In The ApcMin/+ Mouse

Cancer cachexia is a condition associated with the loss of skeletal muscle and adipose tissue mass. The ApcMin/+ mouse is an established model of colorectal cancer that also develops cachexia. IL-6 is necessary for the development of cachexia in the ApcMin/+ mouse. While endurance exercise can reduce polyp number and systemic inflammation in the ApcMin/+ mouse, the affect of exercise on IL-6-induced cachexia in the ApcMin/+ mouse is not known. PURPOSE: The purpose of this study was to determine if 8 weeks of treadmill exercise could repress IL-6-induced cachexia in the ApcMin/+ mouse. METHODS: ApcMin/+ mice were assigned to either 8 weeks of treadmill (6 days/week, 18m/s, 5% grade) exercise or cage control treatments at 6 weeks of age. After 6 weeks of exercise training, circulating IL-6 over-expression was induced by electroporation of a plasmid into the quadriceps while an empty vector served as the control. Body weight, muscle and fat pad weights were recorded at 14 weeks of age. RESULTS: Electroporation increased circulating plasma IL-6 in sedentary control mice (6.7 vs 141 pg/ml) and the exercise group (10.4 vs 111 pg/ml). Sedentary ApcMin/+ mice over-expressing IL-6 lost 10.2% (p < 0.001) of their body mass during the 2 week period. The loss in body weight corresponded to a 13% reduction (p = 0.04) in soleus muscle wet weight and a 45% (p = 0.002) reduction in epididymal fat pad weight. Exercise training prevented the IL-6 induced loss in body weight and maintained soleus muscle and epididymal fat pad weights. CONCLUSION: These data show chronic moderate treadmill exercise in the ApcMin/+ mouse prevents cachexia induced by IL-6 over-expression. Funded by R01CA121249-01A2

Abstract 4172: Multi-parametric characterization of an experimental model of cancer cachexia

Abstract Cachexia is a complex syndrome that is characterized by a massive loss of adipose tissue and skeletal mass. It is encountered in up to 50% of cancer patients and accounts for more than 20% of cancer related deaths. Currently, there is no known cure for cachexia, since mechanisms underlying its manifestation are not defined clearly enough to design effective therapeutic strategies. Here we have used magnetic resonance imaging (MRI) to characterize the vascular properties of cachectic vs. non-cachectic tumors. We have also analyzed the glucose metabolism of these tumors by using [18F]fluorodeoxyglucose (FDG) with positron emission tomography (PET). These studies will provide further insight into the cachectic phenotype that can be used to design treatments to arrest or reverse this condition. We used cachectic (MAC16) and non-cachectic (MAC13) murine colon adenocarcinoma tumors. The cell lines, originally from Dr. Tisdale's laboratory, were obtained from Dr. Sidransky with Dr. Tisdale's permission. Approximately 2 × 106 cells were inoculated in the flank of male SCID mice. MRI studies were performed on a 4.7T Bruker Avance spectrometer. Mice were anesthetized with an i.p. injection of ketamine and acepromazine. For vascular imaging, the tail vein was catheterized before placing the animal in the spectrometer. Multislice relaxation rate maps were obtained by a saturation recovery method combined with fast T1 SNAPSHOT-FLASH imaging. An M0 map with a recovery delay of 7 s was acquired from four 1 mm thick slices through the tumor followed by corresponding images obtained with three relaxation delays (100 ms, 500 ms, and 1 s). The T1 maps were obtained before i.v. injection of albumin-GdDTPA and repeated over a 21 minute period. For PET imaging, mice fasted overnight were injected with 0.2 mCi of FDG. At 60 min post injection, a 15 min static image was acquired over the tumors. Images were decay corrected and reconstructed using 2D OSEM. Cachectic MAC16 tumors induced extensive weight loss, unlike the non-cachectic MAC13 tumors. The difference in the weight of mice became significant within 2 weeks after inoculation. Mice with comparable tumor volumes were imaged 3 to 4 weeks after inoculation. While vascular volumes were not significantly different between the two groups, we did observe significantly lower permeability in the cachectic tumors. Consistent with the MRI data we found significantly lower levels of VEGF mRNA in quantitative-RT-PCR of tumor extracts of MAC16 tumors compared to MAC13 tumors but not in MAC16 cells compared to MAC13 cells. FDG PET imaging revealed increased glycolytic activity in a cachectic MAC16 tumor compared to a non-cachectic MAC13 tumor. These studies are part of our ongoing work to obtain a comprehensive characterization of the cachectic phenotype using noninvasive multi-modality imaging that will allow us to detect cancer-induced cachexia and identify new targets to prevent or reverse this condition. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4172.

Comparison of a bioimpedance monitor with dual-energy x-ray absorptiometry for noninvasive estimation of percentage body fat in dogs

To assess performance of a portable bioimpedance monitor for measurement of body composition in dogs. 24 client-owned dogs. Percentage body fat was measured via dual-energy x-ray absorptiometry (DEXA) and with a portable bioimpedance monitor, and body condition score (BCS) was measured by use of a 9-integer scale. Although the precision of the bioimpedance monitor was good, this varied among dogs. Body position (standing vs sternal) had no effect on bioimpedance results. There was a significant association between results determined via DEXA and bioimpedance, but this association was weaker than between DEXA and BCS. When agreement was assessed via Bland-Altman plot, the bioimpedance monitor under- and overestimated values at high and low body fat percentages, respectively. In 9 dogs, body fat measurements were taken before and after weight loss to determine the proportional loss of tissue mass during weight management. There was a significant difference in the estimated percentage of weight lost as fat between the DEXA and bioimpedance methods. Although percentage body fat measured by use of a portable bioimpedance monitor correlated well with values determined via DEXA, the imprecision and inaccuracy in dogs with high percentage body fat could make the monitor inappropriate for clinical practice.

A Phase II Study of an Herbal Decoction That Includes Astragali Radix for Cancer-Associated Anorexia in Patients With Advanced Cancer

Anorexia and cancer cachexia produce significant loss of adipose tissue and muscle mass and eventually reduce survival in cancer patients. This phase II study was conducted to assess the efficacy and the safety of an herbal decoction with Astragali radix in patients with anorexia in advanced cancer. All patients with histologic evidence of an incurable malignancy had a weight loss of at least 5% during the preceding 6 months and a patient-estimated severe anorexia.The herbal decoction was administered 30 minutes after meals, three times a day for 3 weeks.The score of appetite, body weight, the cytokines, IL-1beta, IL-6, TNF-alpha, and anthropometric measurements were assessed. For the assessment of anorexia, a visual analog scale (VAS: 0 mm = no anorexia, 100 mm = maximal anorexia) was used. Eleven patients were recruited from January, 2007 to January, 2009. The mean age was 59.8 years old. The change in anorexia from baseline with the herbal decoction was significantly different and anorexia was improved (anorexia VAS score, 60 mm vs. 40 mm, p = 0.008). The mean value of the maximal body weight was 55.6 kg and differed significantly from the 54.6 kg at baseline (p = 0.009). Changes in cytokine levels and anthropometric measurements from baseline to the 3rd week were not significant. All toxicities were manageable. Appetite and body weight were improved with the herbal decoction. This herbal decoction shows some potential for management of cancer-related anorexia.

Mitochondrial DNA: An Up‐and‐coming Actor in White Adipose Tissue Pathophysiology

Mitochondrial DNA: An Up‐and‐coming Actor in White Adipose Tissue Pathophysiology

Dietary supplementation with a specific combination of high protein, leucine, and fish oil improves muscle function and daily activity in tumour-bearing cachectic mice

Cancer cachexia is characterised by metabolic alterations leading to loss of adipose tissue and lean body mass and directly compromises physical performance and the quality of life of cancer patients. In a murine cancer cachectic model, the effects of dietary supplementation with a specific combination of high protein, leucine and fish oil on weight loss, muscle function and physical activity were investigated. Male CD2F1 mice, 6–7 weeks old, were divided into body weight-matched groups: (1) control, (2) tumour-bearing, and (3) tumour-bearing receiving experimental diets. Tumours were induced by s.c. inoculation with murine colon adenocarcinoma (C26) cells. Food intake, body mass, tumour size and 24 h-activity were monitored. Then, 20 days after tumour/vehicle inoculation, the animals were killed and muscle function was tested ex vivo. Tumour-bearing mice showed reduced carcass, muscle and fat mass compared with controls. EDL muscle performance and total daily activity were impaired in the tumour-bearing mice. Addition of single nutrients resulted in no or modest effects. However, supplementation of the diet with the all-in combination of high protein, leucine and fish oil significantly reduced loss of carcass, muscle and fat mass (loss in mass 45, 52 and 65% of TB-con, respectively (P<0.02)) and improved muscle performance (loss of max force reduced to 55–64% of TB-con (P<0.05)). Moreover, total daily activity normalised after intervention with the specific nutritional combination (50% of the reduction in activity of TB-con (P<0.05)). In conclusion, a nutritional combination of high protein, leucine and fish oil reduced cachectic symptoms and improved functional performance in cancer cachectic mice. Comparison of the nutritional combination with its individual modules revealed additive effects of the single components provided.

Loss of Total and Visceral Adipose Tissue Mass Predicts Decreases in Oxidative Stress After Weight‐loss Surgery

It is not known whether there are mechanisms linking adipose tissue mass and increased oxidative stress in obesity. This study investigated associations between decreasing general and abdominal fat depots and oxidative stress during weight loss. Subjects were severely obese women who were measured serially at baseline and at 1, 6 (n = 30), and 24 months (n = 18) after bariatric surgery. Total fat mass (FAT) and volumes of visceral (VAT) and subcutaneous abdominal adipose tissue (SAT) were related to plasma concentrations of derivatives of reactive oxidative metabolites (dROMS), a measure of lipid peroxides and oxidative stress. After intervention, BMI significantly decreased, from 47.7 +/- 0.8 kg/m(2) to 43.3 +/- 0.8 kg/m(2) (1 month), 35.2 +/- 0.8 kg/m(2) (6 months), and 30.2 +/- 1.2 kg/m(2) (24 months). Plasma dROMS also significantly deceased over time. At baseline, VAT (r = 0.46), FAT (r = 0.42), and BMI (r = 0.37) correlated with 6-month decreases in dROMS. Similarly, at 1 month, VAT (r = 0.43) and FAT (r = 0.41) correlated with 6-month decreases in dROMS. Multiple regression analysis showed that relationships between VAT and dROMS were significant after adjusting for FAT mass. Increased plasma dROMS at baseline were correlated with decreased concentrations of high-density lipoprotein (HDL) at 1 and 6 months after surgery (r = -0.38 and -0.42). This study found longitudinal associations between general, and more specifically intra-abdominal adiposity, and systemic lipid peroxides, suggesting that adipose tissue mass contributes to oxidative stress.

Cyclooxygenase-2 inhibition reverts the decrease in adiponectin levels and attenuates the loss of white adipose tissue during chronic inflammation

Chronic arthritis leads to a decrease in body weight that is associated with a decrease in skeletal muscle and white adipose tissue mass. We have observed that overactivation of cyclooxygenase-2 (COX-2) is responsible for muscle wasting in arthritic rats. The aim of this work was to study the role of COX-2 in arthritis-induced white adipose tissue mass loss. Arthritis was induced in rats by Freund′s adjuvant injection, and the effect of the COX-2 inhibitor meloxicam on serum concentrations of leptin, adiponectin, insulin and glycerol, as well as on gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor alpha (TNF) and insulin-like growth factor I (IGF-I) in white adipose tissue were determined. Arthritis decreased adipose tissue weight, serum leptin and adiponectin as well as their mRNAs in adipose tissue. Meloxicam administration to arthritic rats increased adipose tissue weight, serum concentrations of adiponectin and its mRNA in adipose tissue, but it did not modify leptin. Arthritis decreased serum insulin and FAS and IGF-I gene expression in adipose tissue. Meloxicam administration did not modify these effects. Serum concentrations of glycerol were decreased in arthritic rats. In control rats, meloxicam administration did not modify serum glycerol or adipose tissue gene expression of HSL. However, in arthritic rats HSL gene expression in adipose tissue was decreased by meloxicam. All these data indicate that COX-2 activation plays a role in the decrease in adiponectin secreted by adipocytes and in the loss in white adipose tissue mass in arthritic rats.

Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death

Supv3L1 is a conserved and ubiquitously expressed helicase found in numerous tissues and cell types of many species. In human cells, SUPV3L1 was shown to suppress apoptotic death and sister chromatid exchange, and impair mitochondrial RNA metabolism and protein synthesis. In vitro experiments revealed binding of SUPV3L1 to BLM and WRN proteins, suggesting a role in genome maintenance processes. Disruption of the Supv3L1 gene in the mouse has been reported to be embryonic lethal at early developmental stages. We generated a conditional mouse in which the phenotypes associated with the removal of exon 14 can be tested in a variety of tissues. Disruption mediated by a Mx1 promoter-driven Cre displayed a postnatal growth delay, reduced lifespan, loss of adipose tissue and muscle mass, and severe skin abnormalities manifesting as ichthyosis, thickening of the epidermis, and atrophy of the dermis and subcutaneous tissue. Using a tamoxifen-activatable Esr1/Cre driver, Supv3L1 disruption resulted in growth retardation and aging phenotypes, including loss of adipose tissue and muscle mass, kyphosis, cachexia, and premature death. Many of the abnormalities seen in the Mx1-Cre mice, such as hyperkeratosis characterized by profound scaling of feet and tail, could also be detected in tamoxifen-inducible Cre mice. Conditional ablation of Supv3L1 in keratinocytes confirmed atrophic changes in the skin and ichthyosis-like changes. Together, these data indicate that Supv3L1 is important for the maintenance of the skin barrier. In addition, loss of Supv3L1 function leads to accelerated aging-like phenotypes.

Cancer cachexia-anorexia syndrome and skeletal muscle wasting

Cancer cachexia-anorexia syndrome and skeletal muscle wastingBackground. Cachexia-anorexia syndrome is a common and important indicator of cancer. It occurs in 30% to 80% of cancer patients. Cachexia means "bad condition" and may be present in the early stages of tumor growth, before any signs of malignancy. Cancer cachexia is a syndrome of progressive body wasting, characterized by loss of adipose tissue and skeletal muscle mass. In most cancer patients, cachexia is characterized by anorexia, which implies a failure of food intake, regulated through a complex system of hormones and neuropeptides. A decline in food intake relative to energy expenditure is a fundamental physiologic derangement leading to cancer associated weight loss. The weight loss in patients with cachexia-anorexia syndrome differs from that in caloric starvation or anorexia nervosa. The pathophysiology of cancer cachexia is not fully understood; however, studies have shown that cytokines are important in the alteration of the carbohydrate, lipid and protein metabolism. Cancer, prolonged bed rest, HIV infection and aging are conditions in which muscle wasting is a common feature. An intervention that may potentially attenuate the progression of muscle wasting in cancer patients is resistance exercise training, defined as multiple repetitions of static or dynamic muscular contractions

Cachexia, survival and the acute phase response

To review current knowledge of the relationship between cytokines, the acute phase response (APR) and the development of cachexia. Cytokines important in the initiation of the APR are also important in the genesis of cachexia. The presence of an APR or high circulating levels of pro-inflammatory cytokines are known to be related to adverse outcome in cancer patients. Studies of host cytokine genotype have demonstrated that specific host cytokine polymorphisms are associated with both the development of cachexia and reduced patient survival. The desire to be able to predict accurately survival in cancer patients has led to the description of various APR-based prognostic scoring systems. Cachexia is an important clinical problem affecting up to two thirds of cancer patients. It results from anorexia and metabolic change and leads to loss of both adipose tissue and lean body mass, particularly in the skeletal muscle compartment. An APR is seen in half of cancer patients at presentation, and is most often determined clinically by raised plasma C-reactive protein concentrations. Adverse outcome and shortened survival have been linked to the presence of an APR. This article explores the cause and consequences of the APR in cancer cachexia.

Changes in body composition during weight loss in obese client-owned cats: Loss of lean tissue mass correlates with overall percentage of weight lost

Obesity is one of the most common medical diseases in cats, but there remains little information on success of weight loss regimes in obese client-owned cats. No information currently exists on body composition changes during weight loss in clinical cases. Twelve obese client-owned cats undertook a weight loss programme incorporating a high-protein low fat diet. Body composition was quantified by dual-energy X-ray absorptiometry, before and after weight loss. Mean (+/-standard deviation) weight loss was 27+/-6.8% of starting weight, and mean rate of weight loss was 0.8+/-0.32% per week. Mean energy allocation during weight loss was 32+/-7.0 kcal/kg target weight. Mean composition of tissue lost was 86:13:1 (fat:lean:bone mineral). The proportion of lean tissue loss was positively associated with overall percentage of weight loss (simple linear regression, r(2)=44.2%, P=0.026). Conventional weight loss programmes produce safe weight loss, but lean tissue loss is an inevitable consequence in cats that lose significant proportions of their starting body weight.

Does repeated burial of skeletal muscle tissue ( Ovis aries) in soil affect subsequent decomposition?

The repeated introduction of an organic resource to soil can result in its enhanced degradation. This phenomenon is of primary importance in agroecosystems, where the dynamics of repeated nutrient, pesticide, and herbicide amendment must be understood to achieve optimal yield. Although not yet investigated, the repeated introduction of cadaveric material is an important area of research in forensic science and cemetery planning. It is not currently understood what effects the repeated burial of cadaveric material has on cadaver decomposition or soil processes such as carbon mineralization. To address this gap in knowledge, we conducted a laboratory experiment using ovine ( Ovis aries) skeletal muscle tissue (striated muscle used for locomotion) and three contrasting soils (brown earth, rendzina, podsol) from Great Britain. This experiment comprised two stages. In Stage I skeletal muscle tissue (150 g as 1.5 g cubes) was buried in sieved (4.6 mm) soil (10 kg dry weight) calibrated to 60% water holding capacity and allowed to decompose in the dark for 70 days at 22 °C. Control samples comprised soil without skeletal muscle tissue. In Stage II, soils were weighed (100 g dry weight at 60% WHC) into 1285 ml incubation microcosms. Half of the soils were designated for a second tissue amendment, which comprised the burial (2.5 cm) of 1.5 g cube of skeletal muscle tissue. The remaining half of the samples did not receive tissue. Thus, four treatments were used in each soil, reflecting all possible combinations of tissue burial (+) and control (−). Subsequent measures of tissue mass loss, carbon dioxide-carbon evolution, soil microbial biomass carbon, metabolic quotient and soil pH show that repeated burial of skeletal muscle tissue was associated with a significantly greater rate of decomposition in all soils. However, soil microbial biomass following repeated burial was either not significantly different (brown earth, podsol) or significantly less (rendzina) than new gravesoil. Based on these results, we conclude that enhanced decomposition of skeletal muscle tissue was most likely due to the proliferation of zymogenous soil microbes able to better use cadaveric material re-introduced to the soil.

Loss of lean tissue mass in adults with CF: an independent predictor of loss of bone mineral density (BMD)

Loss of lean tissue mass in adults with CF: an independent predictor of loss of bone mineral density (BMD)

Longitudinal follow-up of bone mineral density in adults with cystic fibrosis: Loss of BMD correlates with loss of lean tissue mass

Longitudinal follow-up of bone mineral density in adults with cystic fibrosis: Loss of BMD correlates with loss of lean tissue mass

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Adjuvant-induced arthritis is a model of rheumatoid arthritis that induces cachexia. In other cachectic situations, there is an increase in lipolysis resulting in a loss of adipose tissue mass. The aim of this work was to analyse the effect of chronic arthritis, induced by adjuvant injection, on white adipose tissue (WAT). For this purpose, rats were killed 10 days after adjuvant injection, when the first external symptoms appeared, on days 15 and 22 when the external signs of the illness reach their severest level. As arthritis decreases food intake, a pair-fed group was also included. Serum concentrations of insulin, leptin, adiponectin, glycerol and nitrites, as well as gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor alpha and zinc-alpha(2)-glycoprotein (ZAG) were determined. Arthritis decreased food intake between days 5 and 16, but not during the last 5 days of the experiment. There was a marked decrease in relative adipose tissue weight and in serum leptin and adiponectin as well as in their gene expression in WAT in arthritic rats. Arthritis decreased the gene expression of FAS in the WAT. However, none of these effects was found in pair-fed rats. Arthritis did not increase lipolysis, since arthritic rats have lower serum concentrations of glycerol, HSL mRNA in WAT, as well as liver ZAG mRNA than the pair-fed or control rats. These data suggest that in chronic arthritis the decrease in white adipose mass is secondary to a reduced adipose lipogenesis, and this effect is not mainly due to the decrease in food intake.