The impact of weight and fat mass loss and increased physical activity on physical function in overweight, postmenopausal women

Abstract Canine obesity is associated with reduced lifespan and metabolic dysfunction, but can be managed by dietary intervention. This study aimed to determine the effects of restricted feeding of a high-protein, high-fiber (HPHF) diet and weight loss on body composition, physical activity, blood metabolites, and fecal microbiota and metabolites of overweight dogs. Twelve spayed female dogs [age: 5.5±1.1 yr; body weight (BW): 14.8±2.0 kg, body condition score (BCS): 7.9±0.8] were fed a HPHF diet during a 4-wk baseline phase to maintain BW. After baseline (wk 0), dogs were first fed 80% of baseline intake and then adjusted to target 1.5% weekly weight loss for 24 wk. Body composition using dual-energy x-ray absorptiometry and blood samples (wk 0, 6, 12, 18, 24), voluntary physical activity (wk 0, 7, 15, 23), and fresh fecal samples for microbiota and metabolite analysis (wk 0, 4, 8, 12, 16, 20, 24) were measured over time. Microbiota data were analyzed using QIIME 2. All data were analyzed statistically over time using SAS 9.4. After 24 wk, dogs lost 31.2% of initial BW and had 1.43±0.73% weight loss per wk. BCS decreased (P<0.0001) by 2.7 units, fat mass decreased (P<0.0001) by 3.1 kg, and fat percentage decreased (P<0.0001) by 3.1 kg and 11.7% with weight loss. Many serum metabolites and hormones were altered, with triglycerides, leptin, insulin, C-reactive protein, and interleukin-6 decreasing (P<0.05) with weight loss. Relative abundances of fecal Bifidobacterium, Coriobacteriaceae UCG-002, undefined Muribaculaceae, Allobaculum, Eubacterium, Lachnospira, Negativivibacillus, Ruminococcus gauvreauii group, uncultured Erysipelotrichaceae, and Parasutterella increased (P<0.05), whereas Prevotellaceae Ga6A1 group, Catenibacterium, Erysipelatoclostridium, Fusobacterium, Holdemanella, Lachnoclostridium, Lactobacillus, Megamonas, Peptoclostridium, Ruminococcus gnavus group, and Streptococcus decreased (P<0.01) with weight loss. Despite the number of significant changes, a state of dysbiosis was not observed in overweight dogs. Fecal ammonia and secondary bile acids decreased, while fecal valerate increased with weight loss. Several correlations between gut microbial taxa and biological parameters were observed. Our results suggest that restricted feeding of a HPHF diet and weight loss promotes fat mass loss, minimizes lean mass loss, reduces inflammatory marker and triglyceride concentrations, and modulates fecal microbiota phylogeny and activity in overweight dogs.

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Intermittent Fasting and Fat Mass: What Is the Clinical Magnitude?

Obesities ◽

10.3390/obesities2010001 ◽

2022 ◽

Vol 2 (1) ◽

pp. 1-7

Author(s):

Heitor O. Santos

Keyword(s):

Mass Loss ◽

Fat Mass ◽

Clinical Studies ◽

Recent Literature ◽

Energy Restriction ◽

Intermittent Fasting ◽

Reasonable Approach ◽

Treatment Of Obesity ◽

One Year ◽

Fat Mass Loss

Clinical studies addressing the benefits of intermittent fasting (IF) diets have evoked interest in the treatment of obesity. Herein, the overall effects of IF regimens on fat-mass loss are explained in a brief review through a recent literature update. To date, human studies show a reduction in fat mass from 0.7 to 11.3 kg after IF regimens, in which the duration of interventions ranges from two weeks to one year. In light of this, IF regimens can be considered a reasonable approach to weight (fat mass) loss. However, the benefits of IF regimens occur thanks to energy restriction and cannot hence be considered the best dietary protocol compared to conventional diets.

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Effect of a Hypocaloric Diet, Increased Protein Intake and Resistance Training on Lean Mass Gains and Fat Mass Loss in Overweight Police Officers

Annals of Nutrition and Metabolism ◽

10.1159/000012817 ◽

2000 ◽

Vol 44 (1) ◽

pp. 21-29 ◽

Cited By ~ 54

Author(s):

Robert H. Demling ◽

Leslie DeSanti

Keyword(s):

Resistance Training ◽

Mass Loss ◽

Fat Mass ◽

Lean Mass ◽

Police Officers ◽

Protein Intake ◽

Hypocaloric Diet ◽

Fat Mass Loss

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Abstract 17361: How Leptin Harms the Heart in High Fat Diet-Induced Obesity

Circulation ◽

10.1161/circ.142.suppl_3.17361 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Maria Pini

Keyword(s):

Body Weight ◽

Mass Loss ◽

Fat Mass ◽

High Fat Diet ◽

Cardiac Fibroblasts ◽

High Fat ◽

Wide Range ◽

Plasma Leptin ◽

Fat Mass Loss

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

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