Significant Loss Of Body Fat Research Articles

Characterization of Redox Environment and Tryptophan Catabolism through Kynurenine Pathway in Military Divers’ and Swimmers’ Serum Samples

Endurance and resistance exercises, alone or in combination, induce metabolic changes that affect tryptophan (Trp) catabolism. The kynurenine pathway (KP) is the main route of Trp degradation, and it is modulated by the inflammatory and redox environments. Previous studies have shown that KP metabolites work as myokines that mediate the positive systemic effects related to exercise. However, it is poorly understood how different exercise modalities and intensities impact the KP. The aim of this study was to characterize the effect of two different exercise modalities, military diving and swimming, on the KP and the redox environment. A total of 34 healthy men from the Mexican Navy were included in the study, 20 divers and 14 swimmers, who started and stayed in military training consistently during the six months of the study; 12 Mexican men without fitness training were used as the control group. Physical fitness was determined at the beginning and after 6 months of training; criteria included body composition; serum levels of Trp, kynurenine (KYN), kynurenic acid (KYNA) and 3-hydroxykynurenine (3-HK); the glutathione ratio (GSH/GSSG); and malondialdehyde (MDA).. Results showed a significant loss of body fat in both the diver and swimmer groups. Compared with the control group, divers showed a decrease in Trp and 3-HK levels, but no changes were observed in the KYN/Trp, KYNA/Trp or 3-HK/Trp ratios, while swimmers showed a decrease in KYN levels and an increase in the KYNA and 3-HK levels. Additionally, divers showed a decrease in the GSH/GSSG ratio and an increase in MDA levels, in contrast to the swimmers, who showed a decrease in MDA levels and an increase in GSH/GSSG levels. Our findings suggest a differential shift in the KP and redox environment induced by diving and swimming. Swimming promotes an antioxidant environment and a peripheral overactivation of the KP.

1397-P: A Cocoa Butter–Based Ketogenic Diet Fails to Improve Glucose Homeostasis and Promote Weight Loss in Obese Mice

Background: High-fat and very low-carbohydrate based ketogenic diets have gained considerable popularity as a non-pharmacological strategy for treating obesity due to their potential to enhance weight loss and improve glucose homeostasis. However, the effectiveness of a ketogenic diet towards metabolic health is equivocal. Methods: Male and female mice were fed a 60% cocoa butter fat-based high-fat diet for 16-weeks to induce obesity, following which mice were transitioned to either an 85% cocoa butter fat-based ketogenic diet (KD) , a 10% cocoa butter fat-based low-fat diet (LFD) , or maintained on a high-fat diet for an additional 8-weeks. All experimental diets were matched for sucrose and protein content, and contained an identical micronutrient profile, with complex carbohydrates being the primary carbohydrate source in the LFD. Results: The transition to a KD was ineffective at inducing significant body fat loss, improving glucose homeostasis, or enhancing insulin sensitivity in obese male and female mice. Alternatively, obese male and female mice transitioned to a LFD exhibited a marked decrease in body weight, which was primarily attributed to a loss of adiposity, and an improved glucose tolerance during an intraperitoneal glucose tolerance test. Despite the improvements in glucose tolerance, insulin sensitivity remained impaired in obese male mice transitioned to a LFD, whereas it was improved in obese female mice. These salutary actions attributed to a transition to a LFD resulting in beneficial body composition changes and improved glucose tolerance, may in part be due to the trend to mild reductions and increases in food intake and energy expenditure, respectively. Conclusions: Our findings suggest that careful consideration should be taken when consuming a KD as a non-pharmacological strategy for treating obesity, whereas consumption of a diet low in saturated fat and rich in complex carbohydrates imparts numerous beneficial actions. Disclosure A.A.Greenwell: None. G.Lopaschuk: None. R.A.Batran: None. J.R.Ussher: None. C.T.Saed: None. S.Tabatabaei dakhili: None. K.Ho: None. K.Gopal: None. J.S.F.Chan: None. O.Kaczmar: None. S.A.Dyer: None. F.Eaton: None.

ADRB2 gene influences responsiveness to physical exercise programs: A longitudinal study applied to overweight or obese Brazilian children and adolescents.

We aimed to investigate whether the expression levels and polymorphisms in the ADRB2 gene have influenced the anthropometric and cardiometabolic outcomes changes in obese/overweight children submitted to physical exercise programs. This longitudinal study included 197 overweight or obese children aged 10-16years, submitted to physical exercise programs - three sessions per week for 12weeks. Anthropometric and cardiometabolic profile was collected before and after interventions. The ADRB2 gene expression levels were also measured in these two moments in a small intervention group (n=17) and a control group (n=18). Arg16Gly and Gln27Glu polymorphisms were genotyped. A positive correlation between ADRB2 expression and loss of body fat (%) (p=0.038) was observed, which remained after sex and BMI change corrections. Carriers of the Glu27Glu genotype presented a better response to physical exercise programs regarding their triglycerides levels and triglyceride-glucose index (p=0.001 for both). The participants' responsiveness to physical exercise programs showed variation due to the ADRB2 gene expression and the Gln27Glu polymorphism. A more significant loss of body fat was associated with higher levels of ADRB2 expression, and the Glu27Glu genotype was associated with a better cardiometabolic response. The Arg16Gly polymorphism did not show interaction with the responsiveness to physical exercise.

Adipose deficiency and aberrant autophagy in a Drosophila model of MPS VII is corrected by pharmacological stimulators of mTOR

Mucopolysaccharidosis type VII (MPS VII) is a recessively inherited lysosomal storage disorder caused due to β-glucuronidase (β-GUS) enzyme deficiency. Prominent clinical symptoms include hydrops fetalis, musculoskeletal deformities, neurodegeneration and hepatosplenomegaly leading to premature death in most cases. Apart from these, MPS VII is also characterized as adipose storage deficiency disorder although the underlying mechanism of this lean phenotype in the patients or β-GUS-deficient mice still remains a mystery. We addressed this issue using our recently developed Drosophila model of MPS VII (the CG2135-/- fly), which also exhibited a significant loss of body fat. We report here that the lean phenotype of the CG2135−/− larvae is due to fewer number of adipocytes, smaller lipid droplets and reduced adipogenesis. Our data further revealed that there is an abnormal accumulation of autophagosomes in the CG2135−/− larvae due to autophagosome-lysosome fusion defect. Decreased lysosome-mediated turnover also led to attenuated mTOR activity in the CG2135−/− larvae. Interestingly, treatment of the CG2135−/− larvae with mTOR stimulators, 3BDO or glucose, led to the restoration of mTOR activity with simultaneous correction of the autophagy defect and adipose storage deficiency. Our finding thus established a hitherto unknown mechanistic link between autophagy dysfunction, mTOR downregulation and reduced adiposity in MPS VII.

Leukotriene-B4 modulates macrophage metabolism and fat loss in type 1 diabetic mice.

Serum levels of leukotriene-B4 (LTB4) are increased in type 1 diabetes (T1D) and it mediates systemic inflammation and macrophage reprogramming associated with this condition. Herein, we investigated the involvement of LTB4 in adiposity loss, hyperlipidemia, and changes in macrophage metabolism in a mouse model of streptozotocin-induced T1D. LTB4 receptor (BLT1) antagonist u75302 was employed to block LTB4 effects. As expected, hypoinsulinemia in T1D was associated with hyperglycemia, low levels of glucagon, hyperlipidemia, significant body fat loss, and increased white adipose tissue expression of Fgf21, a marker for lipolysis. With the exception of hyperglycemia and hypoglucagonemia, blockade of LTB4 signaling reverted these parameters in T1D mice. Along with hyperlipidemia, macrophages from T1D mice exhibited higher lipid uptake and accumulation. These cells also had enhanced glycolysis and oxidative metabolism and these parameters were dependent on the mitochondrial uncoupling respiration, as evidenced by elevated expression of oxidation markers carnitine palmitoyltransferase and uncoupling protein 1. Interestingly, all these parameters were at least partially reverted in T1D mice treated with u75302. Altogether, these findings suggest that in T1D mice LTB4/BLT1 is involved in the fat loss, hyperlipidemia, and increased macrophage lipid uptake and metabolism with an important involvement of mitochondrial uncoupling activity. These previously unrecognized LTB4/BLT1 functions may be explored in future to therapeutically alleviate severity of hyperlipidemia and systemic inflammation in T1D.

The “Senobi” breathing exercise is recommended as first line treatment for obesity

Neuroadrenergic abnormalities, including a predominant activity of parasympathetic nerve and blunted hormone secretion, are recognized in the overweight patients. This study aimed to examine whether the "Senobi" breathing method, a stretch-breathing exercise that we have developed, could activate or recover sympathetic nervous system activity that leads to the loss of body weight. Forty pre-menopausal women, aged 40 to 50 years, participated in this study. Twenty were healthy and the other 20 were overweight (body mass index>25 and body fat>30%). Sympathetic nerve activity was assessed using equipment that analyzes cardiac-beat variation, and several urinary hormone levels were examined before and 30 min after performing the "Senobi" breathing exercise. The average proportion of sympathetic nerve among healthy women during daytime hours (10:00 AM to 12:00 PM) was 62.6%±2.6%. On the other hand, that of overweight women was 33.5%±0.4%. After 1 min of the "Senobi" breathing, substantial up-regulation of sympathetic nerve activity and increased urinary hormone secretion were observed in the overweight women but not in the healthy controls. Moreover, after repeating the exercise for a month, the obese patients showed significant loss of body fat. The "Senobi" breathing exercise was found to be effective for weight loss in obesity possibly by regulating the autonomic nervous system and the hormone secretion.

3-Iodothyronamine: a novel hormone controlling the balance between glucose and lipid utilisation

3-Iodothyronamine is considered as a derivate of thyroid hormone as a result of enzymatic deiodination and decarboxylation. The physiological role of thyronamine (T1AM) is not known. The aim of this study was to analyze the metabolic response to T1AM in the Djungarian hamster Phodopus sungorus. We measured the influence of T1AM (50 mg/kg) on metabolic rate (VO(2)), body temperature (T (b)) and respiratory quotient (RQ) in this species and in BL/6 mice. T1AM treated hamsters as well as the mice showed a rapid decrease in VO(2) and T (b), accompanied by a reduction of RQ from normal values of about approximately 0.9 to approximately 0.70 for several hours. This indicates that carbohydrate utilisation is blocked by the injection of T1AM and that metabolic pathways are rerouted from carbohydrate to lipid utilisation in response to T1AM. This assumption was further supported by the observation that the treatment of T1AM caused ketonuria and a significant loss of body fat. Our results indicate that T1AM has the potential to control the balance between glucose and lipid utilisation in vivo.

Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC “diet trials”

Objective To compare the effectiveness of four commercial weight loss diets available to adults in the United Kingdom.Design Six month multicentre randomised unblinded controlled trial.Setting Community based sample of otherwise...

Weight loss: the treatment of choice for knee osteoarthritis? A randomized trial

We wanted to assess the effect of rapid diet-induced weight loss on the function of obese, knee osteoarthritis (OA) patients. Eighty patients with knee OA, 89% women (n=71), were recruited. Mean (SD) body-mass index (BMI) was 35.9 (5.1) kg/m(2) and age 62.6 (11.1) years. Patients were randomized to either a low-energy diet (LED 3.4MJ/day), or a control diet (5MJ/day). The LED group had weekly dietary sessions, whereas the control group was given a booklet describing weight loss practices. Changes in body weight and body composition were examined as independent predictors of changes in knee OA symptoms. Symptoms were monitored by the Western Ontario and McMaster Universities' (WOMAC) OA index. The LED and control group lost a mean (SE) of 11.1 (0.6)% and 4.3 (0.6)%, respectively, with a mean difference being 6.8% (95% confidence interval (CI): 5.5 to 8.1%; P<0.0001). The decrease in body fat percent was higher in the LED group, 2.2% (1.5 to 3.0%; P<0.0001). The total WOMAC index improved in the LED group (P<0.0001), but not in the control group (P=0.12), mean difference: -219.3mm (-369.2 to -69.4mm; P=0.005). The 'Number Needed to Treat (NNT)' to ensure an improvement in WOMAC>/=50% was 3.4 (2.1 to 8.8) patients. Changes in total WOMAC index were best predicted by the reduction of body fat percent, with a 9.4% (4.8 to 13.9%) improvement in WOMAC for each percent of body fat reduced (P=0.0005). In our patients with knee OA, a weight reduction of 10% improved function by 28%. LED might be of advantage to control diet because of the rapidity of weight loss and a more significant loss of body fat.

Interventions for visceral adiposity associated with human immunodeficiency virus: application of a method for assessing efficacy.

In addition to lipoatrophy of the subcutaneous fat compartment and lipohypertrophy of the breasts and dorsocervical fat pad, excess visceral fat is considered to be part of human immunodeficiency virus (HIV)-associated lipodystrophy. Because of associations between visceral adiposity and atherosclerotic risk and undesirable clinical and psychological effects, therapies for this morphological alteration are under investigation. The non-HIV literature on the visceral fat effects of various weight-reduction methods provides some insight into the difficulty that lies ahead. We demonstrate the application of a method published by Smith and Zachwieja to 3 studies of HIV that resulted in a significant loss of body fat. The method is meant to control for differences in the initial amount of visceral fat per subcutaneous fat and for absolute weight change. The results show that the body composition differences in HIV may require the development and application of a new method that permits wider variation in fat distribution.

Effects of recombinant human growth hormone on hepatic lipid and carbohydrate metabolism in HIV-infected patients with fat accumulation.

We recently reported that treatment with a pharmacologic dose of recombinant human growth hormone (GH) resulted in a significant loss of body fat and gain in lean tissue in HIV-infected patients with syndromes of fat accumulation. However, insulin-mediated glucose disposal decreased transiently after one month of GH therapy. The present paper focuses on the changes of hepatic carbohydrate and fat metabolism associated with GH treatment in the same subjects. We assessed hepatic insulin sensitivity under both fasting and hyperinsulinemic-euglycemic clamp conditions prior to and after one and six months of GH treatment (3 mg/day) in five patients using stable isotope tracer techniques. Indirect calorimetry, and measurements of lipid concentrations. Fasting endogenous glucose production (EGP) increased significantly at one month (12.0 +/- 0.7 to 14.9 +/- 0.9 micromol/kg/min, P < 0.03), and the increase was sustained at six months of GH treatment (14.0 +/- 1.1 micromol/kg/min, NS). This increase in EGP was driven in part by increased glucogenesis (GNG) (3.5 +/- 0.9 to 5.2 +/- 0.9 and 5.8 +/-1.2 micromol/kg/min, n = 4, P < 0.01 and P < 0.01 at one and six months, respectively); small changes in hepatic glycogenolysis also contributed. Sustained increases in lipolysis and progressive decreases in hepatic fractional de novo lipogenesis (DNL) and triglyceride concentrations occurred with GH treatment. These changes were accompanied by an improved lipid profile with a significant increase in HDL cholesterol and significant decreases in total and LDL cholesterol and triglyceride levels, the latter consistent with the decrease in hepatic DNL. During a hyperinsulinemic-euglycemic glucose clamp, EGP and GNG were markedly suppressed compared to the corresponding time points under fasting conditions, albeit less so when measured after one month of GH treatment. Thus, in HIV-infected patients with abnormal fat distribution, pharmacologic doses of GH improved the overall lipid profile, but worsened glucose homeostasis under both fasting and hyperinsulinemic conditions. The combined implications of these positive and negative metabolic effects for cardiovascular disease risk remain unknown.

The effect of increased adiposity on food intake of juvenile rats

The regulation of feeding by body adiposity, as proposed by the lipostatic theory, has been well demonstrated in adult animals. However, mechanisms controlling long-term feeding in juvenile animals have not been well defined. In this study, increased adiposity was induced in young rats through oral gavage. Four-week-old rats were divided into three groups; ad lib feeding (100%-AL), tubefed 100% (100%-TF) or 150% (150%-TF) of ad lib intake. Animals were tube-fed these levels for one week. At the end of this period, one third of each group were killed and all remaining animals were returned to ad lib feeding for either 4 or 29 days later. During this recovery period, the 150%-TF group had significantly depressed food intakes for the first 4 days in comparison to the 100%-TF group. Afterwards, there were no significant differences between these two groups for the remainder of the study. Overfeeding induced significant increases in total body fat in the 150%-TF group (24.8 grams) in comparison to the 100%-AL group (11.0 grams) and the 100%-TF group (14.0 grams). By day five of recovery, only the 150% group exhibited a significant loss of body fat. Total carcass protein and ash were not different between groups at any period. At day 29 of recovery, there were no treatment differences in carcass weight or fat content. Loss of body fat from the 150%-TF rats was associated with the decline in caloric intake. It appears that food intake is affected by relative adiposity during the dynamic phase of growth.

Pathogenesis of cachexia in cancer. A review and a hypothesis.

The clinical features of cachexia characterized by anorexia, marked asthenia, significant loss of body fat, protein and other components, anemia, water and electrolyte abnormalities and increased basal metabolic rate and energy expenditure despite the reduced dietary intake are just the most obvious manifestations of a profound systemic derangement of the host metabolism. A hypothesis to explain the pathogenesis of cancer cachexia is proposed.

Circulating lipids in surgical patients.

Certain metabolic changes are known to occur in response to surgical trauma. An understanding of these changes is of importance for proper handling of patients during surgery and convalescence. Numerous experimental and clinical studies on various aspects of metabolic response to surgery have been published during recent years, but relatively little work has been done on possible alterations in lipid metabolism as a result of operative trauma. Surgery may be associated with a significant loss of body fat. This is believed to be due to mobilization of depot fat stores for energy. After major surgery some patients are bound to subsist on a relatively deficient caloric intake for a considerable length of time. Intravenous fat emulsions have come into use as a means of supplementing caloric intake in such patients. But, what is known about the state of fat metabolism in a patient undergoing surgery? Is the patient capable of