Vitamins and Hormones Series 

About: Vitamins and Hormones Series is an academic journal. The journal publishes majorly in the area(s): Receptor & Vitamin. Over the lifetime, 1467 publications have been published receiving 55809 citations.

Insulin-like growth factor binding proteins.

Abstract: Publisher Summary This chapter discusses the insulin-like growth factor (IGF) binding proteins—namely, IGF-I and IGF-II The IGFs are purified from human plasma and cell culture medium by virtue of their ability to stimulate the growth of cartilage or cultured fibroblasts, or their insulin-like activity The IGFs are synthesized in many fetal and postnatal tissues and are capable of acting locally IGF-I and IGF-II are single-chain 75-kDa polypeptides that are chemically related to insulin They bind with high affinity to IGF-I receptors that are thought to mediate most of their biological actions The IGF-I receptor is a homolog of the insulin receptor, having a heterotetrameric structure and a tyrosine kinase domain in the cytoplasmic portion of the β-subunit that phosphorylates the receptor and other substrates, and presumably is involved in transmembrane signaling Hybrid receptors consisting of one αβ IGF-I receptor heterodimer and one αβ insulin receptor heterodimer are described IGF-II also binds with high affinity to the IGF-II/Mannose 6-phosphate receptor IGF-II added with the IGF-II/Mannose 6-phosphate receptor stimulated the activation of the guanosine triphosphate (GTP) binding protein G i-2 The IGFs participate in the physiological growth of the developing child, fetus, and embryo

11 beta-Hydroxysteroid dehydrogenase.

Abstract: In mammalian tissues, at least two isozymes of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyze the interconversion of hormonally active C11-hydroxylated corticosteroids (cortisol, corticosterone) and their inactive C11-keto metabolites (cortisone, 11-dehydrocorticosterone). The type 1 and type 2 11 beta-HSD isozymes share only 14% homology and are separate gene products with different physiological roles, regulation, and tissue distribution. 11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid. By contrast, 11 beta-HSD1 acts predominantly as a reductase in vivo, facilitating glucocorticoid hormone action in key target tissues such as liver and adipose tissue. Over the 10 years, 11 beta-HSD has progressed from an enzyme merely involved in the peripheral metabolism of cortisol to a crucial pre-receptor signaling pathway in the analysis of corticosteroid hormone action. This review details the enzymology, molecular biology, distribution, regulation, and function of the 11 beta-HSD isozymes and highlights the clinical consequences of altered enzyme expression.

Release of interleukins and other inflammatory cytokines by human adipose tissue is enhanced in obesity and primarily due to the nonfat cells.

Abstract: The white adipose tissue, especially of humans, is now recognized as the central player in the mild inflammatory state that is characteristic of obesity. The question is how the increased accumulation of lipid seen in obesity causes an inflammatory state and how this is linked to the hypertension and type 2 diabetes that accompanies obesity. Once it was thought that adipose tissue was primarily a reservoir for excess calories that were stored in the adipocytes as triacylglycerols. In times of caloric deprivation these stored lipids were mobilized as free fatty acids and the insulin resistance of obesity was attributed to free fatty acids. It is now clear that in humans the expansion of adipose tissue seen in obesity results in more blood vessels, more connective tissue fibroblasts, and especially more macrophages. There is an enhanced secretion of some interleukins and inflammatory cytokines in adipose tissue of the obese as well as increased circulating levels of many cytokines. The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. The secretion of leptin, on the other hand, by the nonfat cells is negligible. The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. However, on a quantitative basis the vast majority of the TNF-alpha comes from the nonfat cells. Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids.

Regulation of Glucose Uptake by Muscle

Abstract: Publisher Summary It is now recognized that a number of factors can influence the uptake of glucose by muscle. Some are of physiological importance and these include hormones, notably insulin, growth hormone, corticosteroids, and adrenaline and possibly thyroxine and glucagon, and nonhormonal factors such as the availability of oxygen, the contractile activity of the tissue, the concentration of glucose in extracellular water, arid the availability for respiration of other substrates, such as ketone bodies and fatty acids. Other factors that influence glucose uptake arc of interest because of their hypoglycemic effects in diabetic patients and animals, notably salicylate and 2 ,4-dinitrophenol. The uptake of glucose by muscle is a complex process, which is thought to involve, in sequence, passage of the sugar from capillaries to the muscle cell membrane, transfer across the cell membrane, and metabolism within the cell by multienzyme systems with their various cofactors.

Ecdysone receptors and their biological actions.

Abstract: Publisher Summary This chapter discusses the ecdysone receptors and their biological actions. It also summarizes the insect endocrinology and the roles of these steroids in the molting and metamorphosis. Natural hormones that lead to molting and metamorphosis are ecdysones. Molecules whose structures resemble those of the natural hormones are called ecdysteroids. The receptor for ecdysone is a member of the nuclear receptor superfamily that acts as a ligand-dependent transcription factor. The vertebrate steroid hormone receptors act as homodimers whereas the functional ecdysone receptor is always a heterodimer of receptor for ecdysone (EcR) with another member of the nuclear receptor (NR) superfamily, Ultraspiracle, the insect homolog of the vertebrate retinoid X receptor (RXR). Two new technologies promise to transform the environment for investigations of insect hormones, ecdysone receptor, and metamorphosis. The microarrays of expressed sequence tags are constructed (ESTs) and used hybridization to catalog changes in gene expression during metamorphosis. The first technological achievement is reviewed: the complete sequence of the Drosophila genome is obtained and is about to be released. It will be the first complete insect sequence and also the first genomic sequence from an organism that has served as a model for nuclear receptor endocrinology.