| Full text | |
| Author(s): Show less - |
Campolim, Clara Machado
[1]
;
Weissmann, Lais
[2]
;
de Oliveira Ferreira, Clilton Krauess
[1]
;
Zordao, Olivia Pizetta
[2]
;
Segantine Dornellas, Ana Paula
[1]
;
de Castro, Gisele
[2]
;
Zanotto, Tamires Marques
[2]
;
Boico, Vitor Ferreira
[1]
;
Fernandes Quaresma, Paula Gabriele
[2]
;
Ataide Lima, Raquel Patricia
[1]
;
Donato, Jose
[3]
;
Veras, Mariana Matera
[4]
;
Nascimento Saldiva, Paulo Hilario
[4]
;
Kim, Young-Bum
[5]
;
Prada, Patricia Oliveira
[2, 1]
Total Authors: 15
|
| Affiliation: | [1] State Univ Campinas UNICAMP, Sch Appl Sci, Limeira, SP - Brazil
[2] State Univ Campinas UNICAMP, Sch Med Sci, Dept Internal Med, Campinas, SP - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo, SP - Brazil
[4] Univ Sao Paulo, Hosp Clin HCFMUSP, Lab Poluicao Atmosfer Expt LIM05, Fac Med, Sao Paulo, SP - Brazil
[5] Harvard Med Sch, Div Endocrinol Diabet & Metab, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 - USA
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | SCIENTIFIC REPORTS; v. 10, n. 1 JUN 23 2020. |
| Web of Science Citations: | 0 |
| Abstract | |
A previous study demonstrated that a high-fat diet (HFD), administered for one-three-days, induces hypothalamic inflammation before obesity's established, and the long term affects leptin signaling/action due to inflammation. We investigate whether exposure to particulate matter of a diameter of <= 2.5 mu m (PM2.5) in mice fed with a chow diet leads to similar metabolic effects caused by high-fat feeding. Compared to the filtered air group (FA), one-day-exposure-PM2.5 did not affect adiposity. However, five-days-exposure-PM2.5 increased hypothalamic microglia density, toll-like-receptor-4 (Tlr4), and the inhibitor-NF-kappa-B-kinase-epsilon (Ikbke) expression. Concurrently, fat mass, food intake (FI), and ucp1 expression in brown adipose tissue were also increased. Besides, decreased hypothalamic STAT3-phosphorylation and Pomc expression were found after twelve-weeks-exposure-PM2.5. These were accompanied by increased FI and lower energy expenditure (EE), leading to obesity, along with increased leptin and insulin levels and HOMA. Mechanistically, the deletion of Tlr4 or knockdown of the Ikbke gene in the hypothalamus was sufficient to reverse the metabolic outcomes of twelve-weeks-exposure-PM2.5. These data demonstrated that short-term exposure-PM2.5 increases hypothalamic inflammation, similar to a HFD. Long-term exposure-PM2.5 is even worse, leading to leptin resistance, hyperphagia, and decreased EE. These effects are most likely due to chronic hypothalamic inflammation, which is regulated by Tlr4 and Ikbke signaling. (AU) | |
| FAPESP's process: | 17/19703-2 - IMPACT OF THE PERINATAL EXPOSURE TO ENVIRONMENTAL POLLUTANTS IN THE GENESIS OF OBESITY AND DIABETES MELLITUS TYPE 2: METABOLIC AND EPIGENETIC ASPECTS |
| Grantee: | Raquel Patricia Ataíde Lima |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| FAPESP's process: | 17/11518-1 - Study of the effects of atmospheric pollution on obesity genesis: the role of HYPOTALAMIC toll like receptor 4 activation |
| Grantee: | Clara Machado Campolim |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| FAPESP's process: | 17/02983-2 - The role of growth hormone in the brain: relevance for neural functions and in disease |
| Grantee: | Jose Donato Junior |
| Support Opportunities: | Research Projects - Thematic Grants |
| FAPESP's process: | 17/18498-6 - IMPACT OF THE PERINATAL EXPOSURE TO ENVIRONMENTAL POLLUTANTS IN THE GENESIS OF OBESITY AND TYPE 2 DIABETES MELLITUS: METABOLIC AND EPIGENETIC ASPECTS |
| Grantee: | Patrícia de Oliveira Prada |
| Support Opportunities: | Regular Research Grants |