Kombucha tea improves glucose tolerance and reduces hepatic steatosis in obese mice

Carregando...
Imagem de Miniatura
Citações na Scopus
8
Tipo de produção
article
Data de publicação
2022
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
Autores
MOREIRA, Gabriela V.
ARAUJO, Layanne C. C.
MATOS, Sandro L.
CARVALHO, Carla R. O.
Citação
BIOMEDICINE & PHARMACOTHERAPY, v.155, article ID 113660, 10p, 2022
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Nonalcoholic fatty liver disease (NAFLD), often associated with obesity, is becoming one of the most common liver diseases worldwide. It is estimated to affect one billion individuals and may be present in approximately 25% of the population globally. NAFLD is viewed as a hepatic manifestation of metabolic syndrome, with humans and animal models presenting dyslipidemia, hypertension, and diabetes. The gut-liver axis has been considered the main pathogenesis branch for NAFLD development. Considering that foods or beverages could modulate the gastrointestinal tract, immune system, energy homeostasis regulation, and even the gut-liver axis, we conducted an exploratory study to analyze the effects of kombucha probiotic on hepatic steatosis, glucose tolerance, and hepatic enzymes involved in carbohydrate and fat metabolism using a pre-clinical model. The diet-induced obese mice presented glucose intolerance, hyperinsulinemia, hepatic steatosis, increased collagen fiber deposition in liver vascular spaces, and upregulated TNF-alpha and SREBP-1 gene expression. Mice receiving the kombucha supplement displayed improved glucose tolerance, reduced hyperinsulinemia, decreased citrate synthase and phosphofructokinase-1 enzyme activities, downregulated G-protein-coupled bile acid re-ceptor, also known as TGR5, and farnesol X receptor gene expression, and attenuated steatosis and hepatic collagen fiber deposition. The improvement in glucose tolerance was accompanied by the recovery of acute insulin-induced liver AKT serine phosphorylation. Thus, it is possible to conclude that this probiotic drink has a beneficial effect in reducing the metabolic alterations associated with diet-induced obesity. This probiotic beverage deserves an extension of studies to confirm or refute its potentially beneficial effects.
Palavras-chave
NAFLD, Intestinal microbiota, Hepatic steatosis, Insulin resistance, Probiotic
Referências
  1. Abernathy BE, 2021, J NUTR, V151, P352, DOI 10.1093/jn/nxaa376
  2. Arab JP, 2017, HEPATOLOGY, V65, P350, DOI 10.1002/hep.28709
  3. Backhed F, 2004, P NATL ACAD SCI USA, V101, P15718, DOI 10.1073/pnas.0407076101
  4. Behrouz V, 2020, J FOOD SCI, V85, P3611, DOI 10.1111/1750-3841.15367
  5. Bellassoued K, 2015, PHARM BIOL, V53, P1699, DOI 10.3109/13880209.2014.1001408
  6. Bessone F, 2019, CELL MOL LIFE SCI, V76, P99, DOI 10.1007/s00018-018-2947-0
  7. Boulange CL, 2016, GENOME MED, V8, DOI 10.1186/s13073-016-0303-2
  8. Cani PD, 2016, MOL METAB, V5, P743, DOI 10.1016/j.molmet.2016.05.011
  9. Carino A, 2017, SCI REP-UK, V7, DOI 10.1038/srep42801
  10. Chavez-Talavera O, 2017, GASTROENTEROLOGY, V152, P1679, DOI 10.1053/j.gastro.2017.01.055
  11. Chiang JYL, 2013, COMPR PHYSIOL, V3, P1191, DOI 10.1002/cphy.c120023
  12. Chunchai T, 2018, J NEUROINFLAMM, V15, DOI 10.1186/s12974-018-1055-2
  13. CRABTREE B, 1972, BIOCHEM J, V126, P49, DOI 10.1042/bj1260049
  14. Daniel H, 2014, ISME J, V8, P295, DOI 10.1038/ismej.2013.155
  15. Dufresne C, 2000, FOOD RES INT, V33, P409, DOI 10.1016/S0963-9969(00)00067-3
  16. Dutta S, 2016, LIFE SCI, V152, P244, DOI 10.1016/j.lfs.2015.10.025
  17. Cano PG, 2013, OBESITY, V21, P2310, DOI 10.1002/oby.20330
  18. Han HS, 2016, EXP MOL MED, V48, DOI 10.1038/emm.2015.122
  19. Holmes E, 2012, CELL METAB, V16, P559, DOI 10.1016/j.cmet.2012.10.007
  20. Hove KD, 2015, EUR J ENDOCRINOL, V172, DOI 10.1530/EJE-14-0554
  21. Hoyles L, 2018, NAT MED, V24, P1070, DOI 10.1038/s41591-018-0061-3
  22. Hyun J, 2016, FOOD SCI BIOTECHNOL, V25, P861, DOI 10.1007/s10068-016-0142-3
  23. Jung Y, 2019, FOOD SCI BIOTECHNOL, V28, P261, DOI 10.1007/s10068-018-0433-y
  24. Kapp JM, 2019, ANN EPIDEMIOL, V30, P66, DOI 10.1016/j.annepidem.2018.11.001
  25. Kobyliak N, 2018, J GASTROINTEST LIVER, V27, P41, DOI 10.15403/jgld.2014.1121.271.kby
  26. Lakhani SV, 2008, NUTR RES, V28, P293, DOI 10.1016/j.nutres.2008.03.002
  27. Lenzen S, 2014, J BIOL CHEM, V289, P12189, DOI 10.1074/jbc.R114.557314
  28. Li Y, 2011, CELL METAB, V13, P376, DOI 10.1016/j.cmet.2011.03.009
  29. Loomba R, 2021, CELL, V184, P2537, DOI 10.1016/j.cell.2021.04.015
  30. Ma X, 2008, J HEPATOL, V49, P821, DOI 10.1016/j.jhep.2008.05.025
  31. Marcal AC, 2013, BRIT J NUTR, V109, P2154, DOI 10.1017/S0007114512004576
  32. Madrid AM, 2011, DIGEST DIS SCI, V56, P155, DOI 10.1007/s10620-010-1239-9
  33. Leal JM, 2018, CYTA-J FOOD, V16, P390, DOI 10.1080/19476337.2017.1410499
  34. Nagpal R, 2018, J DIABETES RES, V2018, DOI 10.1155/2018/3462092
  35. OPIE LH, 1967, BIOCHEM J, V103, P391, DOI 10.1042/bj1030391
  36. Shin HS, 2010, ARCH PHARM RES, V33, P1425, DOI 10.1007/s12272-010-0917-7
  37. Soares JB, 2010, HEPATOL INT, V4, P659, DOI 10.1007/s12072-010-9219-x
  38. Stefan N, 2019, LANCET DIABETES ENDO, V7, P313, DOI 10.1016/S2213-8587(18)30154-2
  39. Tagliari E, 2017, ABCD-ARQ BRAS CIR DI, V30, P211, DOI 10.1590/0102-6720201700030011
  40. Thiennimitr P., 2018, NUTRITION
  41. Tilg H, 2016, GUT, V65, P2035, DOI 10.1136/gutjnl-2016-312729
  42. Turnbaugh PJ, 2006, NATURE, V444, P1027, DOI 10.1038/nature05414
  43. Vernon G, 2011, ALIMENT PHARM THER, V34, P274, DOI 10.1111/j.1365-2036.2011.04724.x
  44. Wang Y, 2014, J SCI FOOD AGR, V94, P265, DOI 10.1002/jsfa.6245
  45. Wong VWS, 2013, ANN HEPATOL, V12, P256, DOI 10.1016/S1665-2681(19)31364-X
  46. Wu TR, 2019, GUT, V68, P248, DOI 10.1136/gutjnl-2017-315458
  47. Younossi ZM, 2016, HEPATOLOGY, V64, P73, DOI 10.1002/hep.28431
  48. ZAMMIT VA, 1978, BIOCHEM J, V174, P979, DOI 10.1042/bj1740979