ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Evidence has demonstrated that genetic factors play an important role in determining body weight and fat stores in humans and other mammals. In most cases, genetic variation appears to establish an individual’s predisposition to developing obesity, with environmental and psychological factors contributing significantly to the expression of the obese phenotype. Understanding of the genes that contribute to weight and energy homeostasis continues to advance rapidly. During the past year, a more detailed understanding of the mechanisms underlying monogenic causes of obesity in rodents has developed. Studies with transgenic and knock-out mice have identified several new components of central and peripheral weight and energy regulatory pathways. Rare monogenic causes of obesity in humans have demonstrated conservation of basic mechanisms across species and confirmed the relevance of rodent studies to human disease. The value of animal models has been further extended with the demonstration of mutants in mice, fruitflies, and worms that reveal important interactions between genetic and environmental determinants of energy regulation and feeding behavior. Linkage and association studies in both mice and humans have refined the search for the genes that underlie the more subtle and common forms of human obesity, and those that are responsible for the rare and dramatic obesity syndromes that most frequently arise in children. This paper discusses the most significant of these recent developments.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Despite major breakthroughs in the last few years, fundamental questions remain concerning the pathophysiology of leptin action in the brain. How does leptin access its brain targets? Is there any post-receptor defect in the brain of obese individuals? A better understanding of leptin’s neuroendocrine function is also needed. Particularly, how does leptin modulate the release of hypothalamic neuropeptides and pituitary hormones? Progress in these fronts will help to elucidate the role of leptin in the therapy of different hypothalamic/pituitary pathologies, such as delayed puberty, growth defects, or bone metabolism abnormalities.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

This article reviews the changes in body composition and nutrient metabolism in the elderly and how they are affected by macronutrient and micronutrient intake and physical activity. Recent insights into nutrient requirements are cited, as well as the association of nutrition with immune function and neurocognitive function in the elderly. Effects of undernutrition and overnutrition in the elderly are discussed, as well as future directions for insuring the health and functionality of our increasing elderly population.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Gastric procedures are being used more frequently for the treatment of the morbidly obese patient. Associated with varying degrees of intestinal bypass, these operations clinically present a number of nutritional problems. Nutritional support for these patients is an integral aspect of their perioperative care. This includes the use of preoperative weight loss to alter surgical morbidity and improve the effectiveness of laparoscopy, the progression of immediate postoperative diets, and the algorithm for the monitoring and treatment of the postoperative macro-and micronutrient deficiencies. The roles of adjuvant therapy with surgery, including the use of pharmacologic treatment, have not been determined. This underinvestigated area provides limited guidance for the clinician. Most of the recent publications focus on iron, vitamin B12, and calcium depletion. There is considerable room for future investigation into this important area of surgical therapy.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Lifestyle behaviors, including diet modification and physical activity, are needed for weight loss and successful long-term weight loss maintenance. This review highlights recent studies that have suggested the importance of these behavior changes and new strategies that appear effective for modifying diet and exercise. The benefits of food provision and meal replacement strategies are reviewed. Home-based exercise, methods for accumulating exercise through multiple short bouts, and decreasing sedentary behavior have all been studied recently and appear to be promising new approaches to the promotion of physical activity. Finally, the review describes recent research on several new areas related to lifestyle change, including ways to extend therapists’ contact with patients through enhanced social support and Internet interventions, strategies for prevention of weight gain, and the role of physicians in weight loss counseling.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

In the United States, the prevalence of obesity increased by 30% in the decade from 1980 to 1990, and this increase appears to be continuing. Although obesity is recognized as a disease of multiple causes, a virus infection as an etiologic factor has been ignored until now. Five different viruses have been shown to cause obesity in animal models. Canine distemper virus was the first virus reported to cause obesity in mice. This report was followed by a report of Rous-associated virus-7, an avian virus, causing stunting, obesity, and hyperlipidemia in chickens. Next, Borna disease virus, a RNA virus of horses and sheep, was shown to cause obesity in rats. The next two reports are of adenoviruses, SMAM-1, an avian adenovirus that caused obesity in chickens, and Ad-36, a human adenovirus that caused obesity in chickens and mice. Association with human obesity was the unique feature of SMAM-1 and Ad-36. Ad-36 is the only human adenovirus to be implicated in obesity. Although the exact mechanism of virus-induced obesity is unclear, involvement of some viruses in the etiology of obesity urges us to consider a role for other pathogens in etiology of obesity.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Most people with resistance to thyroid hormone have mutant thyroid hormone receptors that interfere with the function of the normal receptor and produce a dominant mode of inheritance. Conversely, thyroid hormone receptor β gene deletion is inherited as a recessive trait. In about 10% of cases, resistance to thyroid hormone manifests in the absence of thyroid hormone receptor gene abnormalities. The clinical manifestations and laboratory abnormalities found in these individuals are not significantly different than those found in patients with thyroid hormone receptor β defects. We propose that the defect must be elsewhere in the pathway of thyroid hormone action.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Apoptosis is a physiologic process of cell death that is central to normal development and occurs in response to a variety of physiologic and pathophysiologic stimuli. In the thyroid, abnormal apoptotic activity may be involved in a variety of diseases such as Hashimoto thyroiditis and Graves disease. Receptor-mediated apoptosis signaling pathways such as those initiated by Fas ligand, tumor necrosis factor, and tumor necrosis factor–related apoptosis-inducing ligand are present and functional in the thyroid. In Hashimoto thyroiditis, which is a typical organ-specific autoimmune disease resulting in thyroid destruction, Fas-mediated apoptosis has been suggested as a mechanism of thyroid follicular cell death. Graves disease is characterized by hyperthyroidism that appears to be caused by autoimmunity. This disorder may be linked to suppression of apoptosis. Apoptosis in thyroid follicular cells may be regulated at multiple levels, including the expression of anti-apoptotic proteins such as Bcl-2. Alterations in the expression of death receptors and ligands by inflammatory cytokines may also play a role in the regulation of apoptosis. These mechanisms may contribute to the pathogenesis of autoimmune thyroid disease.

ISSN:1068-3097    

出版商:OVID    

年代:2000

数据来源: OVID