http://files.farmacognosia-ufsj.webnode.com/200000086-05569074a3/phytochemistry%20anti%20obesidade.pdf

Possible anti-obesity therapeutics from nature--a review.

Some environmental contaminants interact with hormones and may exert adverse consequences as a result of their actions as endocrine disrupting chemicals (EDCs). Exposure in people is typically a result of contamination of the food chain, inhalation of contaminated house dust or occupational exposure. EDCs include pesticides and herbicides (such as dichlorodiphenyl trichloroethane or its metabolites), methoxychlor, biocides, heat stabilisers and chemical catalysts (such as tributyltin), plastic contaminants (e.g. bisphenol A), pharmaceuticals (i.e. diethylstilbestrol; 17α-ethinylestradiol) or dietary components (such as phytoestrogens). The goal of this review is to address the sources, effects and actions of EDCs, with an emphasis on topics discussed at the International Congress on Steroids and the Nervous System. EDCs may alter reproductively-relevant or nonreproductive, sexually-dimorphic behaviours. In addition, EDCs may have significant effects on neurodevelopmental processes, influencing the morphology of sexually-dimorphic cerebral circuits. Exposure to EDCs is more dangerous if it occurs during specific 'critical periods' of life, such as intrauterine, perinatal, juvenile or puberty periods, when organisms are more sensitive to hormonal disruption, compared to other periods. However, exposure to EDCs in adulthood can also alter physiology. Several EDCs are xenoestrogens, which can alter serum lipid concentrations or metabolism enzymes that are necessary for converting cholesterol to steroid hormones. This can ultimately alter the production of oestradiol and/or other steroids. Finally, many EDCs may have actions via (or independent of) classic actions at cognate steroid receptors. EDCs may have effects through numerous other substrates, such as the aryl hydrocarbon receptor, the peroxisome proliferator-activated receptor and the retinoid X receptor, signal transduction pathways, calcium influx and/or neurotransmitter receptors. Thus, EDCs, from varied sources, may have organisational effects during development and/or activational effects in adulthood that influence sexually-dimorphic, reproductively-relevant processes or other functions, by mimicking, antagonising or altering steroidal actions.

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Endocrine disrupters: a review of some sources, effects, and mechanisms of actions on behaviour and neuroendocrine systems

> Abstract Determination of the relative abundance of a specific prokaryote in an environmental sample is of major interest in applied and environmental microbiology. Relative abundance can be calculated using knowledge of SSU rDNA copy number, amount of SSU rDNA in the sample, and a weighted average estimate of the genome sizes for organisms in the original sample. By surveying the literature, we provide estimates of genome size and SSU rDNA copy number for 303 and 101 prokaryotes, respectively. This compilation can be used to make reasonable estimates for a wide range of organisms in the calculation of relative abundance. A statistical analysis suggests that no correlation exists between genome size and SSU rDNA copy number. A phylogenetic analysis is used to offer insights into the evolution of both genome size and SSU rDNA copy number.http://link.springer-ny.com/link/service/journals/00248/bibs/38n2p93.html

Prokaryotic Genome Size and SSU rDNA Copy Number: Estimation of Microbial Relative Abundance from a Mixed Population.

The quality and value of the carcass in domestic meat animals are reflected in its protein and fat content. Preadipocytes and adipocytes are im- portant in establishing the overall fatness of a carcass, as well as being the main contributors to the marbling component needed for consumer preference of meat products. Although some fat accumulation is essential, any excess fat that is deposited into adipose depots other than the marbling fraction is energetically un- favorable and reduces efficiency of production. Hence, this review is focused on current knowledge about the biology and regulation of the important cells of adipose tissue: preadipocytes and adipocytes.

/pdf/board-invited-review-the-biology-and-regulation-of-2nwiw008gc.pdf

Board-invited review: the biology and regulation of preadipocytes and adipocytes in meat animals.

Increased angiotensin II (Ang II), matrix metalloproteinase type II (MMP2), and sympathetic activity accompany age-associated arterial remodeling. To analyze this relationship, we infused a low subpressor dose of Ang II into young (8 months old) rats. This increased carotid arterial MMP2 transcription, translation, and activation, as well as transforming growth factor-β1 activity and collagen deposition. A higher Ang II concentration, which increased arterial pressure to that of old (30 months old) untreated rats, produced carotid media thickening and intima infiltration by vascular smooth muscle cells (VSMCs). Ex vivo, Ang II increased MMP2 activity in carotid rings from young rats to that of untreated old rats. Ang II also increased the ability of early passage VSMCs from young rats to invade a synthetic basement membrane, similar to that of untreated VSMCs from old rats. The MMP inhibitor GM6001 and the AT1 receptor antagonist Losartan inhibited these effects. The α-adrenoreceptor agonist phenylephrine increased arterial Ang II protein, causing MMP2 activation and intima and media thickening. Exposure of young VSMCs to phenylephrine in vitro increased Ang II protein and MMP2 activity to the levels of old VSMCs; Losartan abolished these effects. Thus, Ang II-induced effects on MMP2, transforming growth factor-β1, collagen, and VSMCs are central to the arterial remodeling that accompanies advancing age.

Angiotensin II Activates Matrix Metalloproteinase Type II and Mimics Age-Associated Carotid Arterial Remodeling in Young Rats

In the present study, we performed a differential proteomic analysis using 2-DE combined with MS to clarify the molecular mechanism for the suppressive effect of chitosan oligosaccharides (CO) during differentiation of adipocyte 3T3-L1. Cell differentiation was significantly inhibited by CO at the concentration of 4 mg/mL. Protein mapping of adipocyte homogenates by 2-DE revealed that numerous protein spots were differentially altered in response to CO treatment. Out of 50 identified proteins showing significant alterations, six were up-regulated and 44 were down-regulated by CO treatment in comparison to control mature adipocytes. Among them, most of the proteins are associated with lipid metabolism, cytoskeleton, and redox regulation, in which the levels of farnesyl diphosphate synthetase (FDS), dedicator of cytokinesis 9 (DOCK9), and chloride intracellular channel 1 (CLIC1) were significantly reduced (.two-fold) with CO treatment. These results have not previously been examined in the context of adipogenesis, and thus can be used as novel biomarkers. Taken together with immunoblot analysis, it was concluded that the inhibitory effect of CO on adipocyte differentiation was mediated by C/EBPa and PPARg pathway through significant downregulations of important adipogenic molecules such as fatty acid binding protein and glucose transporter 4.

Proteomic analysis for inhibitory effect of chitosan oligosaccharides on 3T3-L1 adipocyte differentiation.

Currently, the utilization of deep-sea water (DSW) is receiving much attention due to its high productivity, large quantity, and potential for biological application. The 3T3-L1 cell line is a well-established and commonly used in vitro model to assess adipocyte differentiation. Over the course of several days, confluent 3T3-L1 cells can be converted to adipocytes in the presence of an adipogenic cocktail. In this study, the effects of DSW on differentiation adipocyte 3T3-L1 cells were studied. DSW significantly decreased lipid accumulation, a marker of adipogenesis, in a dose-dependent manner. DSW of hardness 1,000 was the most effective for inhibiting adipocyte differentiation without any cytotoxicity. DSW significantly reduced expression mRNA levels of PPARγ and C/EBPα and protein levels of fatty-acid-binding protein and adiponectin. Our results suggest a potential role for DSW as anti-obesity agents by inhibiting adipocyte differentiation mediated through the down-regulated expression of adipogenic transcription factors and adipocyte-specific proteins.

Inhibitory Effect of Deep-sea Water on Differentiation of 3T3-L1 Adipocytes

A high‑fat diet or high‑cholesterol diet (HCD) is a major cause of metabolic diseases, including obesity and diabetes; vascular diseases, including hypertension, stroke and arteriosclerosis; and liver diseases, including hepatic steatosis and cirrhosis. The present study aimed to evaluate the effects of deep sea water (DSW) on rats fed a HCD. DSW decreased HCD‑induced increases in total cholesterol and low‑density lipoprotein (LDL) cholesterol in the blood, and recovered high‑density lipoprotein cholesterol. In addition, DSW decreased levels of liver injury markers, which were increased in response to HCD, including glutamate‑oxaloacetate transaminase, glutamate‑pyruvate transferase and alkaline phosphatase. Lower lipid droplet levels were observed in the livers of rats fed a HCD and treated with DSW at a hardness of 1,500, as compared with those in the HCD only group. Semi‑quantitative reverse transcription‑polymerase chain reaction (RT‑PCR) revealed that mRNA expression levels of fatty acid synthase and sterol regulatory element binding protein‑1c (SREBP‑1c) in rats fed a HCD with DSW were lower compared with the HCD only group. Furthermore, quantitative RT‑PCR revealed that DSW enhanced LDL receptor (LDLR) mRNA expression in a hardness‑dependent manner. Combined, the results of the present study indicated that DSW may reduce HCD‑induced increases in blood and liver lipid levels, indicating that DSW may protect against hypercholesterolemia and non‑alcoholic hepatic steatosis. In addition, the present study demonstrated that DSW‑induced downregulation of lipids in the blood and hepatic lipid accumulation was mediated by enhancement of LDLR expression and suppression of fatty acid synthase and SREBP‑1c.

/pdf/deep-sea-water-improves-hypercholesterolemia-and-hepatic-2vsjrdgxi0.pdf

Deep sea water improves hypercholesterolemia and hepatic lipid accumulation through the regulation of hepatic lipid metabolic gene expression

Age-related changes in matrix metalloproteinase-9 regulation in cultured mouse aortic smooth muscle cells.

We investigated the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expression of synaptic proteins in dissociated E18 rat cortical cells TCDD (0-50 nM) was added to plating media, and cell viability and expression of synaptic proteins were assayed on 4 and 7 days in vitro (DIV), respectively TCDD had no apparent effect on early neurite outgrowth 12 h after plating However, on 4 DIV, cell viability was reduced significantly, and neurons often revealed vacuoles in 20 or 50 nM culture and had limited secondary or higher order dendritic processes in 20 or 50 nM culture Immunoblot analyses of cell homogenates indicated upregulation of NMDA receptor subunits (NR1, NR2A, and NR2B), but downregulation of synaptic organizing proteins (PSD-95, densin-180, and septin6 homologue) and a synapse-enriched enzyme (alphaCaMKII) Changes in the expression of synaptic proteins may be a underlying mechanism for altered synaptic transmission and neuropathy by TCDD

Kyung Soo Nam

Papers

Proteomic analysis for inhibitory effect of chitosan oligosaccharides on 3T3-L1 adipocyte differentiation.

Inhibitory Effect of Deep-sea Water on Differentiation of 3T3-L1 Adipocytes

Deep sea water improves hypercholesterolemia and hepatic lipid accumulation through the regulation of hepatic lipid metabolic gene expression

Age-related changes in matrix metalloproteinase-9 regulation in cultured mouse aortic smooth muscle cells.

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the expression of synaptic proteins in dissociated rat cortical cells.