Chrysin Alters Hypothalamic Levels of Proteins Related to Appetite and Sweet Taste Preferences in Fructose-Fed Rats

Chrysin, a dietary polyphenol, has previously reversed some metabolic syndrome features induced by a high-fructose diet in rats, including altered eating and drinking behavior. However, the effect of this combination in the hypothalamus, which plays a crucial role in regulating appetite, has not been evaluated.

To quantify gene and protein expression of molecules associated with eating and drinking behavior in the hypothalamus after fructose and/or chrysin consumption.

Eight-week-old male Sprague-Dawley rats were randomly assigned to 4 groups: (A) control (tap water), (B) chrysin (100 mg/kg/d, oral), (C) fructose (10% in tap water), and (D) fructose + chrysin (10% fructose in tap water + 100 mg/kg/d chrysin). All rats were fed ad libitum for 18 wk. Hypothalamic protein levels were analyzed by mass spectrometry-based proteomics and gene expression by quantitative reverse transcriptase-polymerase chain reaction. Data were evaluated using one-way analysis of variance followed by Bonferroni correction.

In fructose + chrysin-fed rats, levels of phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit α isoform were reduced by 40%-43% compared with control and fructose groups, whereas signal transducer and activator of transcription 3 levels were 52% lower than in the chrysin group (P < 0.05). Tyrosine 3-monooxygenase and solute carrier family 24 member 4 levels increased to 2- and 1.6-fold, respectively, compared with control. Ubiquitin carboxyl-terminal hydrolase isozyme L1 and L3 levels were 1.2-2-fold higher than those in control and fructose rats, respectively (P < 0.05). Gene expression analysis showed an 84% reduction of pro-opiomelanocortin (P < 0.01) and a 60% reduction in sweet receptor type 2 (P < 0.05) in chrysin-fed compared with fructose-fed rats and an increase (2.8-fold) in sweet taste receptor 3 compared with control (P < 0.01).

The combination of chrysin and fructose induces changes in the gene expression and protein levels of several hypothalamic proteins related to appetite and sweet taste signaling, which may be involved in the altered drinking/eating behavior of these rats.