LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 5 of total 5

Search options

  1. Article ; Online: Abdominal TRPV1 channel desensitization enhances stress-induced hyperthermia during social stress in rats.

    Reis, T O / Noronha, S I S R / Lima, P M A / De Abreu, A R R / Mesquita, L B T / Ferreira, F I / Silva, F C / Chianca-Jr, D A / De Menezes, R C

    Autonomic neuroscience : basic & clinical

    2023  Volume 246, Page(s) 103073

    Abstract: Aims: In rats, stress-induced hyperthermia caused by social interaction depends on brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction. However, the peripheral mechanisms responsible for regulating the level of hyperthermia during ... ...

    Abstract Aims: In rats, stress-induced hyperthermia caused by social interaction depends on brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction. However, the peripheral mechanisms responsible for regulating the level of hyperthermia during social stress are still unknown. The transient receptor potential vanilloid 1 (TRPV1) subfamily, expressed in sensory and visceral neurons, can serve as a thermoreceptor. Here, we tested the hypothesis that the abdominal TRPV1 is essential in regulating stress-induced hyperthermia during social stress.
    Main methods: Male Wistar rats received an intraperitoneal injection of Resiniferatoxin (RTX) - an ultra-potent capsaicin analog, (i.e., to desensitize the TRPV1 channels) or vehicle. Seven days later, we evaluated the effects of abdominal TRPV1 channels desensitization on core body temperature (CBT), brown adipose tissue (BAT) temperature, tail skin temperature, and heart rate (HR) of rats subjected to a social stress protocol.
    Key findings: We found abdominal TRPV1 desensitization increased CBT and BAT temperature but did not change tail skin temperature and HR during rest. However, under social stress, we found that abdominal TRPV1 desensitization heightened the increase in CBT and BAT caused by stress. Also, it abolished the increase in tail skin temperature that occurs during and after social stress. TRPV1 desensitization also delayed the HR recovery after the exposure to the social stress.
    Significance: These results show that abdominal TRPV1 channels desensitization heightens stress-induced hyperthermia, causing heat dissipation during and after social stress, enabling optimal thermal control during social encounters.
    MeSH term(s) Animals ; Male ; Rats ; Capsaicin/pharmacology ; Hyperthermia, Induced ; Rats, Sprague-Dawley ; Rats, Wistar ; TRPV Cation Channels/physiology
    Chemical Substances Capsaicin (S07O44R1ZM) ; TRPV Cation Channels ; Trpv1 protein, rat
    Language English
    Publishing date 2023-01-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020105-9
    ISSN 1872-7484 ; 1566-0702
    ISSN (online) 1872-7484
    ISSN 1566-0702
    DOI 10.1016/j.autneu.2023.103073
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Wheat gluten intake increases weight gain and adiposity associated with reduced thermogenesis and energy expenditure in an animal model of obesity.

    Freire, R H / Fernandes, L R / Silva, R B / Coelho, B S L / de Araújo, L P T / Ribeiro, L S / Andrade, J M O / Lima, P M A / Araújo, R S / Santos, S H S / Coimbra, C C / Cardoso, V N / Alvarez-Leite, J I

    International journal of obesity (2005)

    2016  Volume 40, Issue 3, Page(s) 479–486

    Abstract: Background/objectives: The association between gluten and body weight is inconsistent. Previously, we showed that a gluten-free diet reduces weight gain without changing food intake in mice fed high-fat diets. In the present study, we investigated the ... ...

    Abstract Background/objectives: The association between gluten and body weight is inconsistent. Previously, we showed that a gluten-free diet reduces weight gain without changing food intake in mice fed high-fat diets. In the present study, we investigated the effects of gluten intake on fat metabolism, thermogenesis and energy expenditure in mice fed a standard or high-fat diet.
    Methods: Mice were fed four different experimental diets during 8 weeks: a control-standard diet (CD), a CD added with 4.5% of wheat gluten (CD-G), a high-fat diet (HFD) and a HFD added with 4.5% of wheat gluten (HFD-G). After 8 weeks, the mice received (99m)Tc-radiolabeled gluten orally to study gluten absorption and biodistribution or they underwent indirect calorimetry. After killing, subcutaneous and brown adipose tissues (SAT and BAT) were collected to assess thermogenesis-related protein expression. Lipid metabolism was studied in adipocyte cultures from the four groups.
    Results: Despite having had the same energy intake, CD-G and HFD-G mice exhibited increased body weight and fat deposits compared with their respective controls. (99m)Tc-GLU or its peptides were detected in the blood, liver and visceral adipose tissue, suggesting that gluten can even reach extraintestinal organs. Uncoupling protein-1 expression was reduced in the BAT of HFD-G and in the SAT of CD-G and HFD-G mice. Indirect calorimetry showed lower oxygen volume consumption in CD-G and HFD-G groups compared with their controls. In HFD mice, daily energy expenditure was reduced with gluten intake. Gluten also reduced adiponectin, peroxisome proliferator-activated receptor (PPAR)-α and PPARγ and hormone-sensitive lipase in cultures of isolated adipocytes from HFD mice, whereas in the CD-G group, gluten intake increased interleukin-6 expression and tended to increase that of tumor necrosis factor.
    Conclusions: Wheat gluten promotes weight gain in animals on both HFD and CD, partly by reducing the thermogenic capacity of adipose tissues.
    MeSH term(s) Adipogenesis ; Adiposity ; Animals ; Disease Models, Animal ; Energy Intake ; Energy Metabolism/physiology ; Feeding Behavior ; Gene Expression Regulation ; Glutens ; Lipid Metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/metabolism ; Thermogenesis ; Weight Gain/physiology
    Chemical Substances Glutens (8002-80-0)
    Language English
    Publishing date 2016-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 752409-2
    ISSN 1476-5497 ; 0307-0565
    ISSN (online) 1476-5497
    ISSN 0307-0565
    DOI 10.1038/ijo.2015.204
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article: Interleukin-6 expression and gene polymorphism are associated with severity of periodontal disease in a sample of Brazilian individuals

    Moreira, P.R / Lima, P.M.A / Sathler, K.O.B / Imanishi, S.A.W / Costa, J.E / Gomez, R.S / Gollob, K.J / Dutra, W.O

    Clinical and experimental immunology. 2007 Apr., v. 148, no. 1

    2007  

    Abstract: Interleukin (IL)-6 is an inflammatory mediator involved in bone resorption. G/C polymorphism at position -174 of the IL-6 gene has been reported to influence IL-6 expression, with the G allele associated with higher expression levels. The aims of this ... ...

    Abstract Interleukin (IL)-6 is an inflammatory mediator involved in bone resorption. G/C polymorphism at position -174 of the IL-6 gene has been reported to influence IL-6 expression, with the G allele associated with higher expression levels. The aims of this study were to investigate the expression of IL-6 as well as the incidence of IL-6 (-174) gene polymorphism and their correlation to the severity of periodontitis in Brazilians. Peripheral blood mononuclear cells were collected from 12 non-smoker individuals with periodontitis for evaluation of IL-6 expression using flow cytometry. We observed a positive correlation between the mean clinical attachment loss and intensity of expression of IL-6, in which the greater the attachment loss, the higher the expression of IL-6 (P = 0·007, R² = 0·52). Also, patients with severe periodontitis displayed a higher intensity of IL-6 expression compared to moderate periodontitis (P = 0·04). To determine the occurrence of IL-6 gene polymorphism, DNA was obtained from oral swabs of 209 Brazilian individuals with and without periodontitis. Polymerase chain reaction, restriction endonuclease digestion and electrophoresis were performed, allowing for detection of the IL-6 (-174) polymorphism. We observed that non-smokers with moderate periodontitis (P = 0·05) and control (P = 0·04) groups displayed a higher incidence of the G⁻ genotype when compared to severe periodontitis. This suggests that the G⁻ genotype may represent a protective role in severity of periodontitis. Thus, the increased expression of IL-6 and IL-6 (-174) polymorphism are associated with periodontal disease severity in Brazilian individuals.
    Keywords polymorphism
    Language English
    Dates of publication 2007-04
    Size p. 119-126.
    Publisher Blackwell Publishing Ltd
    Publishing place Oxford, UK
    Document type Article
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1111/j.1365-2249.2007.03327.x
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

  4. Article: Interleukin-6 expression and gene polymorphism are associated with severity of periodontal disease in a sample of Brazilian individuals.

    Moreira, P R / Lima, P M A / Sathler, K O B / Imanishi, S A W / Costa, J E / Gomes, R S / Gollob, K J / Dutra, W O

    Clinical and experimental immunology

    2007  Volume 148, Issue 1, Page(s) 119–126

    Abstract: Interleukin (IL)-6 is an inflammatory mediator involved in bone resorption. G/C polymorphism at position -174 of the IL-6 gene has been reported to influence IL-6 expression, with the G allele associated with higher expression levels. The aims of this ... ...

    Abstract Interleukin (IL)-6 is an inflammatory mediator involved in bone resorption. G/C polymorphism at position -174 of the IL-6 gene has been reported to influence IL-6 expression, with the G allele associated with higher expression levels. The aims of this study were to investigate the expression of IL-6 as well as the incidence of IL-6 (-174) gene polymorphism and their correlation to the severity of periodontitis in Brazilians. Peripheral blood mononuclear cells were collected from 12 non-smoker individuals with periodontitis for evaluation of IL-6 expression using flow cytometry. We observed a positive correlation between the mean clinical attachment loss and intensity of expression of IL-6, in which the greater the attachment loss, the higher the expression of IL-6 (P=0 x 007, R2=0 x 52). Also, patients with severe periodontitis displayed a higher intensity of IL-6 expression compared to moderate periodontitis (P=0 x 04). To determine the occurrence of IL-6 gene polymorphism, DNA was obtained from oral swabs of 209 Brazilian individuals with and without periodontitis. Polymerase chain reaction, restriction endonuclease digestion and electrophoresis were performed, allowing for detection of the IL-6 (-174) polymorphism. We observed that non-smokers with moderate periodontitis (P=0 x 05) and control (P=0 x 04) groups displayed a higher incidence of the G genotype when compared to severe periodontitis. This suggests that the G genotype may represent a protective role in severity of periodontitis. Thus, the increased expression of IL-6 and IL-6 (-174) polymorphism are associated with periodontal disease severity in Brazilian individuals.
    MeSH term(s) Adolescent ; Adult ; Aged ; Cross-Sectional Studies ; Female ; Flow Cytometry/methods ; Genetic Predisposition to Disease ; Genotype ; Humans ; Interleukin-6/blood ; Interleukin-6/genetics ; Leukocytes, Mononuclear/immunology ; Male ; Middle Aged ; Periodontitis/genetics ; Periodontitis/immunology ; Polymorphism, Genetic ; Severity of Illness Index
    Chemical Substances Interleukin-6
    Language English
    Publishing date 2007-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1111/j.1365-2249.2007.03327.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Cura chirurgica delle malattie mentali (psico-chirurgia).

    LIMA, P M A

    Minerva medica

    1950  Volume 41, Issue 36, Page(s) 122–127

    Title translation Surgical treatment of mental psychosurgical) diseases.
    MeSH term(s) Humans ; Psychosurgery
    Language Undetermined
    Publishing date 1950-07-21
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 123586-2
    ISSN 1827-1669 ; 0026-4806
    ISSN (online) 1827-1669
    ISSN 0026-4806
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top