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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Plant Physiol. 2002 Jun;129(2):661-77.
Transcriptional profiling reveals novel interactions between wounding, pathogen, abiotic stress, and hormonal responses in Arabidopsis.

Cheong YH, Chang HS, Gupta R, Wang X, Zhu T, Luan S.

Department of Plant and Microbial Biology, University of California-Berkeley, Berkeley, CA 94720, USA.

Mechanical wounding not only damages plant tissues, but also provides pathways for pathogen invasion. To understand plant responses to wounding at a genomic level, we have surveyed the transcriptional response of 8,200 genes in Arabidopsis plants. Approximately 8% of these genes were altered by wounding at steady-state mRNA levels. Studies of expression patterns of these genes provide new information on the interactions between wounding and other signals, including pathogen attack, abiotic stress factors, and plant hormones. For example, a number of wound-responsive genes encode proteins involved in pathogen response. These include signaling molecules for the pathogen resistance pathway and enzymes required for cell wall modification and secondary metabolism. Many osmotic stress- and heat shock-regulated genes were highly responsive to wounding. Although a number of genes involved in ethylene, jasmonic acid, and abscisic acid pathways were activated, many in auxin responses were suppressed by wounding. These results further dissected the nature of mechanical wounding as a stress signal and identified new genes that may play a role in wounding and other signal transduction pathways.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12068110&dopt=Abstract

Alcohol Clin Exp Res. 2002 Jun;26(6):848-55.
Maternal dietary ethanol consumption is associated with hypertriglyceridemia in adult rat offspring.

Pennington JS, Shuvaeva TI, Pennington SN.

Department of Comparative Medicine, Brody School of Medicine, East Carolina University, Greenville, North Carolina 27858, USA. penningtonsail.ecu.edu

BACKGROUND: The consumption of significant amounts of alcohol (ethanol, EtOH) may markedly increase serum triglyceride levels. This study describes a significant increase in fasting serum triglyceride (TG) levels in adult male rats whose mothers consumed EtOH. The hypertriglyceridemia occurred although the offspring never directly consumed EtOH and had consumed only rat chow for the preceding 14 months. Furthermore, both male and female adult offspring had an additional, significant increase in TG levels if their mothers consumed EtOH and experienced stress (restraint) during the pregnancy. METHODS: Harlan-derived Sprague Dawley female rats were dosed during pregnancy with EtOH via a liquid diet, and their offspring were compared with offspring of mothers who were either fed ad libitum or pair-fed the liquid diet without EtOH. At birth, the offspring of EtOH mothers exhibited no visible abnormalities except reduced weight, and all offspring were surrogate fostered within 48 hr of birth to mothers who had consumed commercial rat chow throughout their pregnancy. After weaning, all offspring consumed only commercial rat chow, and they were examined over the next 14 months for changes in triglyceride homeostasis as a function of maternal alcohol intake. RESULTS: Adult male offspring of mothers that consumed EtOH during their pregnancy had significant increases in fasting serum triglycerides associated with an increase in the very low density lipoprotein serum fraction. Acute administration of insulin to the offspring of all maternal dietary groups resulted in a rapid clearing of the serum triglycerides, and there were no differences in basal or heparin-releasable lipoprotein lipase activity between any of the progeny. Castration of the male offspring of EtOH-treated mothers prevented the development of elevated TG levels. Administration of testosterone to littermate female offspring increased circulating TG levels compared with testosterone-treated offspring of pair-fed mothers. EtOH-consuming mothers who also underwent five periods of restraint-induced stress (approximately 10 min each session) produced offspring whose fasting serum TG levels were higher than those whose mothers consumed EtOH but experienced no restraint or who experienced restraint but no EtOH. Maternal stress significantly reduced lipoprotein lipase activity in some offspring treatment groups, but the changes did not correspond to changes in the serum TG levels of the offspring. That is, maternal restraint-induced stress was associated with a loss of heparin-releasable lipoprotein lipase activity by male progeny from pair-fed and EtOH-fed mothers and the female offspring of ad libitum-fed and EtOH-fed mothers. CONCLUSIONS: Although serum triglycerides increased with age in all offspring, the increase was much more pronounced in the progeny of mothers who consumed EtOH during their pregnancy. The hypertriglyceridemia was significantly more pronounced in the male offspring and in female offspring treated with testosterone. Castration of male offspring inhibited the hypertriglyceridemia development, which suggests that male sex hormones may play a role in the development of this condition. Maternal EtOH consumption coupled with maternal restraint-induced stress significantly increased the level of hypertriglyceridemia in both male and female offspring compared with offspring whose mothers experienced restraint but no EtOH or EtOH with no restraint. If this study models the human condition, the results could represent an unrecognized risk factor in a number of adult disease states hypothesized to be associated with hypertriglyceridemia, such as cardiovascular disease, hypertension, and diabetes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12068254&dopt=Abstract

Horm Behav. 2002 Dec;42(4):472-83.
Prenatal stress alters reproductive responses of rats in behavioral estrus and paced mating of hormone-primed rats.

Frye CA, Orecki ZA.

Department of Psychology, University at Albany-SUNY, 1400 Washington Avenue, Albany, New York 12222, USA. cafrynsunix.albany.edu

Adult female offspring of dams exposed to gestational stress (prenatal stress, PNS) may show altered reproductive behavior, exploration in novel environments, and/or social interactions than do their non-PNS counterparts. These behavioral differences may be more readily observed in a seminatural, paced mating paradigm, in which females have greater control of their sexual contacts, than in a standard mating situation. Adult offspring of dams exposed to restraint and lights for 45 min on Gestational Days 14-20 (PNS) were compared with those not subjected to stress (non-PNS, control condition). The motor, reproductive, and sociosexual behaviors of hormone-primed (Experiment 1) or cycling adult offspring in behavioral estrus (Experiment 2) were examined following 20 min of restraint stress under bright lights (postnatal stress). Hormone-primed PNS rats displayed less motor behavior in a novel arena than did non-PNS rats. In a standard mating test, hormone-primed PNS females tended to be more aggressive toward the male than were non-PNS rats. In a seminatural mating situation, hormone-primed PNS females showed increased avoidance behavior, such as longer latencies to the initial intromission, greater return latencies following mounts and intromissions, and more exiting subsequent to mounts and intromissions, than did non-PNS rats. PNS rats in behavioral estrus had decreased incidence and intensity of lordosis, and fewer solicitation behaviors, in both standard or paced mating situations, in which latency to and number of mounts were also increased. Thus, hormone-primed PNS rats exposed to restraint showed more avoidance behaviors in paced mating situations, while cycling PNS rats in behavioral estrus had greater disruption of reproductive responses in standard or paced mating paradigms than did non-PNS control rats.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12488113&dopt=Abstract

Nat Med. 2002 Jul;8(7):731-7. Epub 2002 Jun 17.
Diet-induced insulin resistance in mice lacking adiponectin/ACRP30.

Maeda N, Shimomura I, Kishida K, Nishizawa H, Matsuda M, Nagaretani H, Furuyama N, Kondo H, Takahashi M, Arita Y, Komuro R, Ouchi N, Kihara S, Tochino Y, Okutomi K, Horie M, Takeda S, Aoyama T, Funahashi T, Matsuzawa Y.

Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan.

Here we investigated the biological functions of adiponectin/ACRP30, a fat-derived hormone, by disrupting the gene that encodes it in mice. Adiponectin/ACRP30-knockout (KO) mice showed delayed clearance of free fatty acid in plasma, low levels of fatty-acid transport protein 1 (FATP-1) mRNA in muscle, high levels of tumor necrosis factor-alpha (TNF-alpha) mRNA in adipose tissue and high plasma TNF-alpha concentrations. The KO mice exhibited severe diet-induced insulin resistance with reduced insulin-receptor substrate 1 (IRS-1)-associated phosphatidylinositol 3 kinase (PI3-kinase) activity in muscle. Viral mediated adiponectin/ACRP30 expression in KO mice reversed the reduction of FATP-1 mRNA, the increase of adipose TNF-alpha mRNA and the diet-induced insulin resistance. In cultured myocytes, TNF-alpha decreased FATP-1 mRNA, IRS-1-associated PI3-kinase activity and glucose uptake, whereas adiponectin increased these parameters. Our results indicate that adiponectin/ACRP30 deficiency and high TNF-alpha levels in KO mice reduced muscle FATP-1 mRNA and IRS-1-mediated insulin signaling, resulting in severe diet-induced insulin resistance.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12068289&dopt=Abstract

Nat Med. 2002 Jul;8(7):738-42. Epub 2002 Jun 17.
Inhibition of gastric inhibitory polypeptide signaling prevents obesity.

Miyawaki K, Yamada Y, Ban N, Ihara Y, Tsukiyama K, Zhou H, Fujimoto S, Oku A, Tsuda K, Toyokuni S, Hiai H, Mizunoya W, Fushiki T, Holst JJ, Makino M, Tashita A, Kobara Y, Tsubamoto Y, Jinnouchi T, Jomori T, Seino Y.

Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Secretion of gastric inhibitory polypeptide (GIP), a duodenal hormone, is primarily induced by absorption of ingested fat. Here we describe a novel pathway of obesity promotion via GIP. Wild-type mice fed a high-fat diet exhibited both hypersecretion of GIP and extreme visceral and subcutaneous fat deposition with insulin resistance. In contrast, mice lacking the GIP receptor (Gipr(-/-)) fed a high-fat diet were clearly protected from both the obesity and the insulin resistance. Moreover, double-homozygous mice (Gipr(-/-), Lep(ob)/Lep(ob)) generated by crossbreeding Gipr(-/-) and obese ob/ob (Lep(ob)/Lep(ob)) mice gained less weight and had lower adiposity than Lep(ob)/Lep(ob) mice. The Gipr(-/-) mice had a lower respiratory quotient and used fat as the preferred energy substrate, and were thus resistant to obesity. Therefore, GIP directly links overnutrition to obesity and it is a potential target for anti-obesity drugs.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12068290&dopt=Abstract

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