LAUSR

Consumption of high-fructose corn syrup (HFCS) in the diet is a causal factor in the development of abdominal obesity; however, the molecular mechanism behind this association is still up for debate. This study evaluated the metabolic disturbances that are caused by HFCS on adipose tissue as well as the possibility of kefir as a therapy to prevent these metabolic disturbances. Male Wistar rats were divided into four groups: control, kefir, HFCS, and HFCS+kefir. HFCS (20%, w/v ) was given in drinking water and kefir (1 mL/100 g body weight) by gastric gavage daily for 8 weeks. Levels of insulin signaling, inflammation, and apoptosis-associated proteins of adipose tissues were determined with Western blot and immunohistochemical techniques. Gene expressions were evaluated with semi-quantitative real-time polymerase chain reaction (qRT-PCR). The indirect terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method was used to assess changes in apoptotic cells, and hematoxylin/eosin staining to determine adipocyte number and diameter. Accordingly, HFCS boosted protein kinase B (Akt) and p-Akt while reducing nuclear factor κB (NF-κB), and tumor necrosis factor alpha (TNFα) levels and kefir treatment restored Akt induction in HFCS-treated rats despite raising NF-κB, and TNFα. Increased expression of Akt and B-cell lymphoma-2 gene ( Bcl2 ) was contrasted with decreased expression of Nfkb, Tnfa, tumor protein 53 gene ( p53 ), and caspase-8 gene ( Casp8 ). Furthermore, while there was a marked reduction in TUNEL-positive cells in the HFCS group, the number of such cells was greater in the HFCS+kefir group. These results show that HFCS intake suppresses apoptosis in adipose tissues, which may be responsible for tissue development and abdominal obesity and may be reversed with kefir administration due to the activation of apoptosis-associated genes and proteins.