Explore the vast range of titles available.

Chromium has been studied since the end of the 19th century, when carcinogenic effects of hexavalent Cr were discovered. Essentiality of trivalent Cr was demonstrated in 1959; Cr3+ has been studied in humans and laboratory animals since the 1970s and it is only since the 1990s that Cr has been studied as an essential element in livestock animals with the same intensity. Trivalent Cr is essential to normal carbohydrate, lipid and protein metabolism. It is biologically active as part of an oligopeptide - chromodulin - potentiating the effect of insulin by facilitating insulin binding to receptors at the cell surface. Cr absorption is low, ranging between 0.4 and 2.0% for inorganic compounds while the availability of organic Cr is more than 10 times higher. Absorbed Cr circulates in blood bound to the beta-globulin plasma fraction and is transported to tissues bound to transferrin. Absorbed Cr is excreted primarily in urine, by glomerular filtration; a small amount is excreted through perspiration, bile and in milk. This review describes Cr metabolism, the different biological functions of Cr and symptoms of Cr deficiency.

▪ Abstract  Desaturation of a fatty acid first involves the enzymatic removal of a hydrogen from a methylene group in an acyl chain, a highly energy-demanding step that requires an activated oxygen intermediate. Two types of desaturases have been identified, one soluble and the other membrane-bound, that have different consensus motifs. Database searching for these motifs reveals that these enzymes belong to two distinct multifunctional classes, each of which includes desaturases, hydroxylases, and epoxidases that act on fatty acids or other substrates. The soluble class has a consensus motif consisting of carboxylates and histidines that coordinate an active site diiron cluster. The integral membrane class contains a different consensus motif composed of histidines. Biochemical and structural similarities between the integral membrane enzymes suggest that this class also uses a diiron cluster for catalysis. Soluble and membrane enzymes have been successfully re-engineered for substrate specificity and reaction outcome. It is anticipated that rational design of these enzymes will result in new and desired activities that may form the basis for improved oil crops.

Recent data have identified leptin as an afferent signal in a negative-feedback loop regulating the mass of the adipose tissue. High leptin levels are observed in obese humans and rodents, suggesting that, in some cases, obesity is the result of leptin insensitivity. This hypothesis was tested by comparing the response to peripherally and centrally administered leptin among lean and three obese strains of mice: diet-induced obese AKR/J, New Zealand Obese (NZO), and A(y). Subcutaneous leptin infusion to lean mice resulted in a dose-dependent loss of body weight at physiologic plasma levels. Chronic infusions of leptin intracerebroventricularly (i.c.v.) at doses of 3 ng/hr or greater resulted in complete depletion of visible adipose tissue, which was maintained throughout 30 days of continuous i.c.v. infusion. Direct measurement of energy balance indicated that leptin treatment did not increase total energy expenditure but prevented the decrease that follows reduced food intake. Diet-induced obese mice lost weight in response to peripheral leptin but were less sensitive than lean mice. NZO mice were unresponsive to peripheral leptin but were responsive to i.c.v. leptin. A(y) mice did not respond to subcutaneous leptin and were 1/100 as sensitive to i.c.v. leptin. The decreased response to leptin in diet-induced obese, NZO, and A(y) mice suggests that obesity in these strains is the result of leptin resistance. In NZO mice, leptin resistance may be the result of decreased transport of leptin into the cerebrospinal fluid, whereas in A(y) mice, leptin resistance probably results from defects downstream of the leptin receptor in the hypothalamus

It is proposed that an important function of leptin is to confine the storage of triglycerides (TG) to the adipocytes, while limiting TG storage in nonadipocytes, thus protecting them from lipotoxicity. The fact that TG content in nonadipocytes normally remains within a narrow range, while that of adipocytes varies enormously with food intake, is consistent with a system of TG homeostasis in normal nonadipocytes. The facts that when leptin receptors are dysfunctional, TG content in nonadipocytes such as islets can increase 100-fold, and that constitutively expressed ectopic hyperleptinemia depletes TG, suggest that leptin controls the homeostatic system for intracellular TG. The fact that the function and viability of nonadipocytes is compromised when their TG content rises above or falls below the normal range suggests that normal homeostasis of their intracellular TG is critical for optimal function and to prevent lipoapoptosis. Thus far, lipotoxic diabetes of fa/fa Zucker diabetic fatty rats is the only proven lipodegenerative disease, but the possibility of lipotoxic disease of skeletal and/or cardiac muscle may require investigation, as does the possible influence of the intracellular TG content on autoimmune and neoplastic processes.

Leptin is currently believed to control body composition largely, if not entirely, via hypothalamic receptors that regulate food intake and thermogenesis. Here we demonstrate direct extraneural effects of leptin to deplete fat content of both adipocytes and nonadipocytes to levels far below those of pairfed controls. In cultured pancreatic islets, leptin lowered triglyceride (TG) content by preventing TG formation from free fatty acids (FFA) and by increasing FFA oxidation. In vivo hyperleptinemia, induced in normal rats by adenovirus gene transfer, depleted TG content in liver, skeletal muscle, and pancreas without increasing plasma FFA or ketones, suggesting intracellular oxidation. In islets of obese Zucker Diabetic Fatty rats with leptin receptor mutations, leptin had no effect in vivo or in vitro. The TG content was approximately 20 times normal, and esterification capacity was increased 3- to 4-fold. Thus, in rats with normal leptin receptors but not in Zucker Diabetic Fatty rats, nonadipocytes and adipocytes sterify FFA, store them as TG, and later oxidize them intracellularly via an \"indirect pathway\" of intracellular fatty acid metabolism controlled by leptin. By maintaining insulin sensitivity and preventing islet lipotoxicity, this activity of leptin may prevent adipogenic diabetes

Cold shock elicits an immediate rise in cytosolic tree calcium concentration ([Ca2+]cyt) in both chilling-resistant Arabidopsis and chilling-sensitive tobacco (Nicotiana plumbaginifolia). In Arabidopsis, lanthanum or EGTA caused a partial inhibition of both cold shock [Ca2+]cyt elevation and cold-dependent kin1 gene expression. This suggested that calcium influx plays a major role in the cold shock [Ca2+]cyt response and that an intracellular calcium source also might be involved. To investigate whether the vacuole (the major intracellular calcium store in plants) is involved, we targeted the calcium-dependent photoprotein aequorin to the cytosolic face of the vacuolar membrane. Cold shock calcium kinetics in this microdomain were consistent with a cold-induced vacuolar release of calcium. Treatment with neomycin or lithium, which interferes with phosphoinositide cycling, resulted in cold shock [Ca2+]cyt kinetics consistent with the involvement of inositol trisphosphate and inositide phosphate signaling in this response. We also investigated the effects of repeated and prolonged low temperature on cold shock [Ca2+]cyt. Differences were observed between the responses of Arabidopsis and N. plumbaginifolia to repeated cold stimulation. Acclimation of Arabidopsis by pretreatment with cold or hydrogen peroxide caused a modified calcium signature to subsequent cold shock. This suggests that acclimation involves modification of plant calcium signaling to provide a \"cold memory\"

Fructan is a general term used for any carbohydrate in which one or more fractosyl-fructose link constitutes the majority of osidic bonds. This review focuses on the fate of inulin-type fructans (namely native chicory inulin, oligofructose produced by the partial enzymatic hydrolysis of chicory inulin, and synthetic fructans produced by enzymatic synthesis from sucrose) in the gastrointestinal tract, as well as on their systemic physiological effects on mineral absorption, carbohydrate and lipid metabolism, hormone balance, and nitrogen homeostasis. The scientific evidence for the functional claims of inulin-type fructans is discussed, as well as their potential application in risk reduction of disease, namely constipation, infectious diarrhea, cancer, osteoporosis, atherosclerotic cardiovascular disease, obesity, and non-insulin dependent diabetes

The activation of defense genes in tomato plants has been shown to be mediated by an octadecanoic acid-based signaling pathway in response to herbivore attack or other mechanical wounding. We report here that a tomato mutant (JL5) deficient in the activation of wound-inducible defense genes is also compromised in resistance toward the lepidopteran predator Manduca sexta (tobacco hornworm). Thus, we propose the name defenseless1 (def1) for the mutation in the JL5 line that mediates this altered defense response. In experiments designed to define the normal function of DEF1, we found that def1 plants are detective in defense gene signaling initiated by prosystemin overexpression in transgenic plants as well as by oligosaccharide (chitosan and polygalacturonide) and polypeptide (systemin) elicitors. Supplementation of plants through their cut stems with intermediates of the octadecanoid pathway indicates that def1 plants are affected in octadecanoid metabolism between the synthesis of hydroperoxylinolenic acid and 12-oxo-phytodienoic acid. Consistent with this defect, def1 plants are also compromised in their ability to accumulate jasmonic acid, the end product of the pathway, in response to wounding and the aforementioned elicitors. Taken together, these results show that octadecanoid metabolism plays an essential role in the transduction of upstream wound signals to the activation of antiherbivore plant defenses

The young larvae of insects living on dry food produce large amounts of water by the metabolic combustion of dietary lipids. The metabolic production of water needed for larval growth, previously known as hypermetabolic responses to juvenile hormone (JH), is associated with a 10 to 20-fold increase in the rate of O2 consumption (10,000 microL O2/g/h in contrast to the usual rate of 500 microL O2/g/h). Growing and moulting larvae are naturally hypermetabolic due to the endogenous release of JH from the corpora allata. At the last, larval-pupal or larval-adult moult there is no JH and as a consequence the metabolic rate is much lower and the dietary lipid is not metabolized to produce water but stored in the fat body. At this developmental stage, however, a hypermetabolic response can be induced by the exogenous treatment of the last larval instars with a synthetic JH analogue. In D. vulpinus, the JH-treated hypermetabolic larvae survive for several weeks without moulting or pupating. In T. castaneum and G. mellonella, the JH-treated hypermetabolic larvae moult several times but do not pupate. All these larvae consume dry food and the hypermetabolic response to JH is considered to be a secondary feature of a hormone, which is produced by some subordinated endocrine organ. The organ is most probably the controversial prothoracic gland (PG), which is a typical larval endocrine gland that only functions when JH is present. According to our hypothesis, PG activated by JH releases an adipokinetic superhormone, which initiates the conversion of dietary lipid into metabolic water. This type of metabolic combustion of dietary lipid produces large quantities of endothermic energy, which is dissipated by the larvae in the form of heat. Thermovision imaging revealed that the body of hypermetabolic larvae of G. mellonella can be as hot as 43 deg C or more. In contrast, the temperature of \"cold\" normal last instar larvae did not differ significantly from that of their environment. It is highly likely that thermovision will facilitate the elucidation of the currently poorly understood hormonal mechanisms that initiate the production of metabolic water essential for the survival of insects that live in absolutely dry conditions.

Sustained hyperleptinemia of 8 ng/ml was induced for 28 days in normal Wistar rats by infusing a recombinant adenovirus containing the rat leptin cDNA (AdCMV-leptin). Hyperleptinemic rats exhibited a 30-50% reduction in food intake and gained only 22 g over the experimental period versus 115-132 g in control animals that received saline infusions or a recombinant virus containing the beta-galactosidase gene (AdCMV-beta Gal). Body fat was absent in hyperleptinemic rats, whereas control rats pair-fed to the hyperleptinemic rats retained approximately 50% body fat. Further, plasma triglycerides and insulin levels were significantly lower in hyperleptinemic versus pair-fed controls, while fatty acid and glucose levels were similar in the two groups, suggestive of enhanced insulin sensitivity in the hyperleptinemic animals. Thus, despite equivalent reductions in food intake and weight gain in hyperleptinemic and pair-fed animals, identifiable fat tissue was completely ablated only in the former group, raising the possibility of a specific lipoatrophic activity for leptin