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Abdominal or visceral fat comprises fat deposits between the liver and kidneys that are packed into the abdominal cavity. This fat is distinct from subcutaneous and intramuscular fat because it is primarily visceral and includes several adipose depots. Historically, such fat has a played a key role in survival in times of famine. As described in the book, such fat is subject to lifestyle man- agement as well as to accumulation.


Appetite-regulating gut hormones, work, diet, and physical activity in adults, children, and adolescents have all been described as factors that affect abdominal fat accumulation. Tarantino describes the efficacy of physical activity in treating nonalcoholic fatty liver dis- ease. Its actions in specific populations, for example the elevated hypertension of African-Americans, are defined and explained by Hornbuckle. Von Gruenigen shows how fat plays a role in cancer survivorship, while Clement reviews massive obesity and its consequences. Clearly, and historically, lifestyle factors are major fac- tors that affect abdominal fat; these are defined by Suliga with Gomez-Martinez in their review of the role of phys- ical activity in abdominal obesity in adolescents. Therapies including surgery and sleeve gastrostomy are reviewed by Ruiz-Tovar, while the beneficial effects of supplemental magnesium are defined by Kokot. Fat is constantly being stored and released from adi- pose tissue. Storage in adipose tissue is regulated by insulin and stimulated by high serum glucose. Thus, fat cells have an important role in maintaining triglyceride and free fatty acid levels. However, abdominal fat is more prone to inducing insulin resistance; therefore, central obesity is a marker of impaired glucose tolerance as a risk factor for many obesity-related diseases. Gasevic et al. show that adipose tissue affects insulin resistance and is further modified by ethnicity. In addition, Rossi and colleagues describe visceral fat as key to ectopic fat accumulation, while Leblanc and Poirier discuss how high blood pressure risk is lessened by reducing visceral obesity. Finally, Prasad defines the problems of advanced glycation end-products in relation to adiposity.


Understanding abdominal obesity will promote its modification and prevention, thus reducing chronic dis- ease levels. Under standard conditions, adipose depots provide feedback on hunger and dietary needs to the central nervous system. A variety of biochemical, physi- ological, and food-regulated mechanisms that alter abdominal obesity and thus disease risk are reviewed. Maeda identifies glucagon-like peptide 1 as an agonist of visceral fat adiposity and appetite. Castonguay defines the role of fructose in hypertriglyceridemia and obesity. Dietary foods play key roles in visceral fat accumulation and its removal. The effects of intermittent fasting ver- sus daily calorie restriction on visceral fat loss are com- pared by Trepanowski and Varady. Laurant and colleagues show that gender and exercise, which both modulate cytokines, affect obesity and thus heart dis- ease. Stress-induced eating also affects obesity, and Finch and Tomiyama describe relevant physiological and behavioral stress responses. Campbell and cowork- ers review fructose-induced hypertriglyceridemia as a cause of abdominal obesity that can be modified by changes in food intake. Yoshinaga describes how the gender and lifestyle of individuals and their parents combine to modify obesity. Adipose tissues play important roles in health; their primary role is as a reserve of lipids needed to provide energy. Fat tissues consist of about 86% fat, and a variety of different cell types regulate fat accumulation. Lipolysis is modulated by lipolytic β-adrenergic receptors and antilipolysis is regulated by α2A adrenergic receptors. Dietary foods and supplements can play critical roles in modifying and preventing such fat accumulation. Park describes several types of soy protein and fermented soypastes that can reduce visceral obesity. Reviews by the Pimentel and Bautista-Castaño groups describe the roles of alcohol, coffee, and bread in modifying obesity through various mechanisms, including immu- nomodulation of inflammation, which is obesity induced. As Nagai and Takatsu review in humans and Masternak in animal models, these mechanisms are important in metabolic disorders associated with chronic diseases. Castonguay and coauthors describe appetite




and reward signals in the brain, with sugar being a major mediator, as shown by magnetic resonance imaging. Additionally, the effects of dietary supplements on fat regulation and thus visceral obesity are an important focus of this book. A stringent vegan diet with dietary restriction produces significant weight loss. A supplement containing flaxseed components changes visceral obesity, inflammation, lipids, and chronic hypertension, as Park summarizes. Damms-Machado shows that nutritional deficiencies in obese patients are a common condition, which are additionally impacted by bariatric operations, like sleeve gastrectomy. Miyashita and Hosokawa show the importance of plant carotenoids as nutraceutical therapies for visceral obesity. Other macromolecules and foods are modulators of visceral fat and play a key role in a host of diseases, including diabetes, insulin resistance, cardiovascular disease, inflammation, and other obesity-related health problems. Pal and coauthors describe a role for psyllium as a therapy for obesity comorbidities. Karl and McKeown describe the role of whole grain (with its intrinsic fiber) in obesity prevention, while Pal defines a similar role for dietary whey protein. Vajro and coworkers describe the role of other complex carbohydrates known as probiotics in treating hepatic obesity and related diseases. Dinner carbohydrates, if used as described by Madar and col- leagues, produce weight loss and have other effects on visceral fat. Citrus is a food that, as Mukai describes in animal models and humans, changes visceral fat accu- mulation. Lipids are the major modulators of fat. Tan

describes the effects of dietary fatty acids on weight, fat mass and abdominal fat. Park shows that conjugated lin- oleic acid benefits human health by controlling weight. Finally, D’Antona reviews the current evidence that amino acid supplementation affects obesity. Free fatty acids are released from lipoproteins by enzymes and enter adipocytes to be reassembled into triglycerides for storage. Through regulating adipose tissues in visceral fat, different cell types (primarily adipocytes, fibroblasts, macrophages, lymphocytes, and endothelial cells) can have wide-ranging effects on health. Matikainen describes the role of fibroblast growth factor 21 in regu- lating energy metabolism in adipose tissues to promote health. Qi discusses how polymorphisms in the gene encoding neuropeptide Y (and other genes) affect central obesity. Finally, Garaulet defines site-specific adipose tis- sue fatty acid composition and its role in the regulation of abdominal obesity. In conclusion, the authors describe how factors that affect the current abdominal obesity epidemic will pro- vide major benefits by preventing chronic diseases, espe- cially heart, vascular, and diabetic diseases. A broad range of disciplines are involved in dealing with the con- sequences of excessive abdominal fat, including cardiol- ogy, diabetes research, endocrinology, exercise physiology, and studies focusing on lipids, metabolism, nutrition, and obesity. We describe how abdominal obe- sity, a major cause of mortality and morbidity in much of the world through its associated diseases, can be regu- lated by food and dietary therapies.