ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

The high pediatric obesity prevalence requires continued examination of the causes of energy imbalance among youth and attention to childhood obesity treatment and prevention strategies. The literature regarding the causes of primary childhood obesity remains inconclusive. Most interventions for childhood obesity are behavioral, with evidence of long-term efficacy associated with intensive family-based behavioral weight control treatment. Recent advances in pharmacologic and surgical interventions for adult obesity have prompted their recent preliminary investigation among children. Behavioral interventions continue to be modified to attempt to improve efficacy and generalizability across the spectrum of children seeking treatment with overweight. School-based programs to reduce obesity incidence have also received recent attention and evaluation.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Among children and adolescents in the United States, both obesity and type 2 diabetes are more prevalent in black and Hispanic subjects. This review summarizes research to date regarding ethnic differences in body composition, body fat distribution, metabolism, pubertal timing, and endocrine status that may contribute to observed disparities in obesity and associated diseases. Research indicates that black children and adolescents have greater bone mineral content and bone mineral density than their white, Hispanic, and Asian counterparts. Similar results have been found at and during puberty. Cross-sectional studies have yielded discrepant results regarding ethnic differences in soft tissue mass. It appears that white children have greater intra-abdominal adipose tissue than black children. Studies on differences in adiposity between black and white subjects report conflicting results. Data do indicate greater fat mass among Hispanic children and adolescents versus white and black subjects. In most studies undertaken, circulating insulin-like growth factor I levels are elevated in black versus white and Hispanic prepubertal children. However, variation in circulating insulin-like growth factor I (free or bound) does not explain ethnic differences in body composition. Insulin, particularly after a glucose challenge, is higher among black versus white subjects, and may be responsible for lower rates of lipolysis and perhaps greater adipose tissue accrual among black subjects. Limited data suggest that estradiol is higher in black versus white subjects. Numerous data indicate that resting energy expenditure is lower among black versus white subjects. Data regarding physical activity are less clear but indicate that at least some populations of black children are less physically active than white children. Whether ethnic differences in resting or physical activity-related energy expenditure contribute to differences in obesity or disease risk remains to be determined.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Growth hormone has an important role in childhood growth, but growth hormone is also detectable from early gestation, suggesting a role in fetal development and metabolism. In early postnatal life, infants who have been growth restrictedin uterohave abnormal patterns of growth hormone secretion with what appears to be evidence of growth hormone resistance, whereas in later childhood, growth hormone deficiency is often observed. Recent studies using high doses of growth hormone in short small for gestational age children have demonstrated increases in growth rate whether or not these children have classical growth hormone deficiency. The benefits are in terms not only of height but also of body composition and psychosocial function. However, the risk of side effects and long-term complications, such as increased insulin resistance, need to be assessed carefully, especially in people who have a family history of type 2 diabetes or the metabolic syndrome in later life.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Medical treatment for congenital adrenal hyperplasia caused by 21-hydroxylase deficiency consists of glucocorticoids and mineralocorticoids. In theory, these drugs allow physiologic regulation of the hypothalamic-pituitary-adrenal axis and maintenance of sodium balance. In practice, exogenous steroid treatment cannot precisely mimic endogenous secretion. Consequences of inappropriate treatment include perturbation of growth, inappropriately timed puberty, female virilization, and potential pituitary, adrenal, and gonadal tumors. Several experimental regimens have been tested attempting to avoid such complications.Surgical repair of ambiguous genitalia in females has been criticized for lack of long-term outcome tracking; newer techniques may yield improved results. In light of the serious psychologic consequences of genital ambiguity, prenatal treatment aimed at ameliorating virilization has been practiced. Two decades of experience indicate favorable outcomes with no apparent permanent adverse effects. This article reviews the current standard of care for patients with congenital adrenal hyperplasia and discusses novel therapeutic approaches meant to enhance quality of life.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Gastrin is a gastrointestinal regulatory peptide that plays a key role in the physiologic regulation of gastric acid secretion. In addition to this important biologic property, numerous studies have documented the trophic effects of both amidated and precursor gastrin peptides on the mucosa of the gastrointestinal tract. Gastrin stimulates not only the growth of normal gastrointestinal epithelial cells but also neoplastic cells in the alimentary tract and pancreas and in extraintestinal sites. Prolonged hypergastrinemia has been found to be a significant risk factor for the development of certain gastrointestinal malignancies. These studies all have suggested a potential role for gastrin in the pathophysiology of these malignancies of the gastrointestinal tract, whereby not only elevated levels of circulating gastrin but also tumor-derived gastrin may provide a stimulus for tumor growth. This review discusses the trophic properties, concentrating on two sites in the gastrointestinal tract, the colon and esophagus. Because gastrin appears to stimulate the proliferation of gastrointestinal and other malignancies, a pharmacologic means for preventing the development of neoplastic cellular hyperproliferation could be developed by inhibiting its expression. Ultimately, gastrin receptor antagonists and the suppression of antral gastrin expression may prove beneficial in decreasing tumor growth and ultimately in preventing malignant transformation throughout the gastrointestinal tract.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Cholecystokinin is a classical gastrointestinal hormone secreted from endocrine cells of the small intestine on ingestion of a meal. It plays a major role in the coordination of many processes involved in the ingestion, digestion, and absorption of nutrients. In addition, cholecystokinin is produced by nerves of the peripheral nervous system and brain, where it functions as a neuroregulator. Since its discovery, important milestones in understanding the physiology and pathophysiology of cholecystokinin include (1) elucidation of its chemical composition and amino acid sequence, (2) development of assays for measuring blood levels of the hormone, (3) cloning of the cDNA and gene encoding cholecystokinin, (4) characterization of the cholecystokinin receptor, and (5) creation of novel cholecystokinin receptor agonists and antagonists. New molecular technologies continue to bring forward new insights into understanding of the biology of cholecystokinin. The current review places into context recent discoveries that impact understanding of the role of cholecystokinin in human health and disease.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Gastrointestinal regulatory peptides have long been known to play an important role in postprandial release of insulin, and glucose-dependent insulinotropic polypeptide is one of two incretins that has been thoroughly investigated. Within the last few years, great progress has been made in understanding the physiologic properties of glucose-dependent insulinotropic polypeptide and its potential use as a therapeutic modality for type 2 diabetes mellitus and obesity. Although glucose-dependent insulinotropic polypeptide possesses insulinotropic properties, its insulin-stimulatory effect is diminished in type 2 diabetic patients, but the mechanisms for this observation remain unclear. Recent studies have suggested a possible genetic defect in meal-stimulated glucose-dependent insulinotropic polypeptide release in diabetic patients and their first-degree relatives, but other mechanisms, including a decrease in glucose-dependent insulinotropic polypeptide receptor number on the pancreatic islet &bgr; cells, shorter glucose-dependent insulinotropic polypeptide half-life, and chronic desensitization of the glucose-dependent insulinotropic polypeptide receptor because of elevated serum glucose-dependent insulinotropic polypeptide levels, may also contribute to this phenomenon. Moreover, the glucose-dependent insulinotropic polypeptide receptor is expressed in adipose tissue, and glucose-dependent insulinotropic polypeptide stimulates lipoprotein lipase activityin vitro, suggesting a potent role of glucose-dependent insulinotropic polypeptide in modulating fat metabolism. In glucose-dependent insulinotropic polypeptide receptor knockout mice, triglyceride synthesis in the adipocyte was found to be significantly impaired. Furthermore, glucose-dependent insulinotropic polypeptide receptor knockout mice did not develop obesity or insulin resistance when fed a high-fat diet. These data indicate that glucose-dependent insulinotropic polypeptide may govern the disposition of fat in the adipose tissue, and they suggest that a glucose-dependent insulinotropic polypeptide antagonist may be useful in preventing obesity.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Mammalian bombesin-like peptides are a small number of regulatory peptides that exert their broad range of biologic functions through specific, high-affinity binding to their respective G protein–coupled receptors, the bombesin receptors. Bombesin-like peptides are widely expressed in the central nervous system and gastrointestinal tract, where important physiologic functions include regulation of satiety, thermoregulation, smooth muscle contraction, and the release of other peptide hormones. Both bombesin-like peptides and their respective bombesin receptors are found aberrantly expressed in some human malignancies, where they may initiate intracellular signals of cell proliferation, differentiation, and migration through autocrine and paracrine mechanisms. This article reviews the molecular biology of bombesin-like peptides and their specific bombesin receptors, and relevant intracellular signaling events in human cancers. Furthermore, clinical applications are summarized, because specific gastrin-releasing peptide receptor antagonists and novel radiolabeled compounds are now introduced as potential tools for the diagnosis and treatment of human cancers bearing functional gastrin-releasing peptide receptors.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID