Conference on 'Nutrition and age-related muscle loss, sarcopenia and cachexia' The first reports of accurate skeletal muscle mass measurement in human subjects appeared at about the same time as introduction of the sarcopenia concept in the late 1980s. Since then these methods, computed tomography and MRI, have been used to gain insights into older (i.e. anthropometry and urinary markers) and more recently developed and refined methods (ultrasound, bioimpedance analysis and dual-energy X-ray absorptiometry) of quantifying regional and total body skeletal muscle mass. The objective of this review is to describe the evolution of these methods and their continued development in the context of sarcopenia evaluation and treatment. Advances in these technologies are described with a focus on additional quantifiable measures that relate to muscle composition and 'quality'. The integration of these collective evaluations with strength and physical performance indices is highlighted with linkages to evaluation of sarcopenia and the spectrum of related disorders such as sarcopenic obesity, cachexia and frailty. Our findings show that currently available methods and those in development are capable of non-invasively extending measures from solely 'mass' to quality evaluations that promise to close the gaps now recognised between skeletal muscle mass and muscle function, morbidity and mortality. As the largest tissue compartment in most adults, skeletal muscle mass and aspects of muscle composition can now be evaluated by a wide array of technologies that provide important new research and clinical opportunities aligned with the growing interest in the spectrum of conditions associated with sarcopenia.
Caenorhabditis elegans is a small free-living nematode that lives in temperate soil environments. It has been widely employed as an animal model in research involving obesity, aging, and neurodegenerative diseases, including Alzheimer's disease, because of its various advantages, such as small size, large number of progeny, completely sequenced genome, and short life span, over traditional animal models of vertebrates. These benefits contribute to an ideal research model organism. In this review, we provide an introduction to C. elegans and its applications in obesity, aging, and Alzheimer's disease studies, with the aim of stimulating scientists to use C. elegans as an experimental model in various fields of research.
Caenorhabditis elegans (C. elegans) is a small nematode that conserves 65% of the genes associated with human disease, has a 21-day lifespan, reproductive cycles of 3 days, large brood sizes, lives in an agar dish and does not require committee approvals for experimentation. Research using C. elegans is encouraged and a Caenorhabditis Genetics Center (CGC, Minnesota) is funded by the National Institutes of Health-National Center for Research Resources. Many genetically manipulated strains of C. elegans are available at nominal cost from the CGC. Studies using the C. elegans model have explored insulin signaling, response to dietary glucose, the influence of serotonin on obesity, satiety, feeding and hypoxia-associated illnesses. C. elegans has also been used as a model to evaluate potential obesity therapeutics, explore the mechanisms behind single gene mutations related to obesity and to define the mechanistic details of fat metabolism. Obesity now affects a third of the US population and is becoming a progressively more expensive public health problem. Faster and less expensive methods to reach more effective treatments are clearly needed. We present this review hoping to stimulate interest in using the C. elegans model as a vehicle to advance the understanding and future treatment of obesity.
Excess adiposity is the main phenotypic feature that defines human obesity and that plays a pathophysiological role in most chronic diseases. Measuring the amount of fat mass present is thus a central aspect of studying obesity at the individual and population levels. Nevertheless, a consensus is lacking among investigators on a single accepted “reference” approach for quantifying fat mass in vivo. While the research community generally relies on the multicomponent body-volume class of “reference” models for quantifying fat mass, no definable guide discerns among different applied equations for partitioning the four (fat, water, protein, and mineral mass) or more quantified components, standardizes “adjustment” or measurement system approaches for model-required labeled water dilution volumes and bone mineral mass estimates, or firmly establishes the body temperature at which model physical properties are assumed. The resulting differing reference strategies for quantifying body composition in vivo leads to small but under some circumstances important differences in the amount of measured body fat. Recent technological advances highlight opportunities to expand model applications to new subject groups and measured components such as total body protein. The current report reviews the historical evolution of multicomponent body volume-based methods in the context of prevailing uncertainties and future potential.
Low-cost 3D Kinect-based imaging systems have the potential for providing automated accurate anthropometric and related body measurements for relatively large components; further hardware and software developments may be able to improve system small-component resolution.
Obesity is a growing global public health dilemma. The objective of this project is to develop and validate a screening mechanism for bioactive compounds that may reduce body fat and promote health. Resistant starch (RS) reduces body fat in rodents. Amylose starch that has a high content of RS, endogenous compounds obtained from the ceca of amylose starch fed mice (fermented RS), and individual short-chain fatty acids (SCFA) were tested. The Caenorhabditis elegans model and Nile red staining were selected to determine the intestinal fat deposition response to bioactive components. The fluorescence intensity of Nile red was reduced to 76.5% (amylose starch), 78.8% (fermented RS), 63.6% (butyrate), or 28-80% (SCFAs) of controls, respectively (P < 0.001). The reduced intestinal fat deposition suggests reduced food intake or increased energy expenditure. C. elegans is a practical animal model to screen for bioactive compounds that may prevent or treat obesity.
The prevalence of obesity is growing, is driving an increase in the prevalence of diabetes, and is creating a major public health crisis in the United States. Lifestyle and behavior therapy rarely give durable weight loss. There are few medications approved for the treatment of obesity. Those that exist are limited in efficacy and using them in combination does not result in greater weight loss. Surgical treatments for obesity are effective and give durable weight loss, but are accompanied by measurable morbidity and mortality. Several pacing approaches are being tried and are an outgrowth of pacing for gastroparesis. The Transcend(R) pacemaker blocks vagal efferents and delays gastric emptying, giving a 40% loss of excess body weight, if certain screening procedures are employed. The Tantulus pacemaker is still in development but increases antral muscular contractions and delays gastric emptying by stimulation during the absolute refractory period. Weight loss has been 30% of excess body weight, and glycohemoglobin decreased 1.6% in a trial of obese type 2 diabetes. Stimulation to the subdiaphragmatic sympathetics, vagal nerve stimulation with or without unilateral vagotomy, and intestinal pacing are other approaches that are still being evaluated preclinically. Clearly a safe, effective, and durable treatment for obesity is desperately needed. Electrical pacing of the gastrointestinal tract is promising therapeutically, and because pacemakers work through different mechanisms, combining pacemaker treatments may be possible. Rapid progress is being made in the field of electrical stimulation as a treatment for obesity and even greater progress can be expected in the foreseeable future.
In addition to their fermentable dietary fiber and the soluble β-glucan fiber, oats have unique avenanthramides that have anti-inflammatory and antioxidant properties that reduce coronary heart disease in human clinical trials. We hypothesized that oat consumption will increase insulin sensitivity, reduce body fat, and improve health span in Caenorhabditis elegans through a mechanism involving the daf-2 gene, which codes for the insulin/insulin-like growth factor-1–like receptor, and that hyperglycemia will attenuate these changes. Caenorhabditis elegans wild type (N2) and the null strains sir-2.1, daf-16, and daf-16/daf-2 were fed Escherichia coli (OP50) and oat flakes (0.5%, 1.0%, or 3%) with and without 2% glucose. Oat feeding decreased intestinal fat deposition in N2, daf-16, or daf-16/daf-2 strains (P < .05); and glucose did not affect intestinal fat deposition response. The N2, daf-16, or sir-2.1 mutant increased the pharyngeal pumping rate (P < .05), a surrogate marker of life span, following oat consumption. Oat consumption increased ckr-1, gcy-8, cpt-1, and cpt-2 mRNA expression in both the N2 and the sir-2.1 mutant, with significantly higher expression in sir-2.1 than in N2 (P < .01). Additional glucose further increased expression 1.5-fold of the 4 genes in N2 (P < .01), decreased the expression of all except cpt-1 in the daf-16 mutant, and reduced mRNA expression of the 4 genes in the daf-16/daf-2 mutant (P < .01). These data suggest that oat consumption reduced fat storage and increased ckr-1, gcy-8, cpt-1, or cpt-2 through the sir-2.1 genetic pathway. Oat consumption may be a beneficial dietary intervention for reducing fat accumulation, augmenting health span, and improving hyperglycemia-impaired lipid metabolism.
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