leptin and chrysin

The study of interaction mechanism between chrysin and leptin was investigated by various spectroscopic techniques and atom force microscope. The ultraviolet spectrum presents a red shift in 200-220 nm after chrysin upon. And there is a structure alternative showed in 270 nm when the concentration ratio of chrysin and leptin in 10-15. From the fluorescence spectrum, it was found that chrysin could combine with leptin in physiological condition. The binding constant (Ka) values, at 298 K and 310 K, were (0.41±0.05)×10⁶ and (3.26±0.46)×10⁶ L·mol⁻¹, and the binding site number were 1.02±0.04 and 0.51±0.01, respectively. The atom force microscope results showed that the dimension of leptin molecules became more swollen after binding with chrysin because of the hydrophobicity. These results demonstrate that the mechanism of chrysin and leptin interaction could play a role in leptin adjust in human body, and it could provide a new aspect for the study of obesity treatment.

Topics: Binding Sites; Flavonoids; Humans; Leptin; Microscopy, Atomic Force; Spectrum Analysis

Obesity is known to be a risk factor for colon carcinogenesis. Although there are several reports on the chemopreventive abilities of dietary flavonoids in chemically induced colon carcinogenesis, those have not been addressed in an obesity-associated carcinogenesis model. In the present study, the effects of 3 flavonoids (chrysin, quercetin and nobiletin) on modulation of the occurrence of putative preneoplastic lesions, aberrant crypt foci (ACF), and beta-catenin-accumulated crypts (BCACs) in the development of colon cancer were determined in male db/db mice with obesity and diabetic phenotypes. Male db/db mice were given 3 weekly intraperitoneal injections of azoxymethane (AOM) to induce the ACF and BCAC. Each flavonoid (100ppm), given in the diet throughout the experimental period, significantly reduced the numbers of ACF by 68-91% and BCAC by 64-71%, as well as proliferation activity in the lesions. Clinical chemistry results revealed that the serum levels of leptin and insulin in mice treated with AOM were greater than those in the untreated group. Interestingly, the most pronounced suppression of development of preneoplastic lesions and their proliferation were observed in the quercetin-fed group, in which the serum leptin level was lowered. Furthermore, quercetin-feeding decreased leptin mRNA expression and secretion in differentiated 3T3-L1 mouse adipocytes. These results suggest that the present dietary flavonoids are able to suppress the early phase of colon carcinogenesis in obese mice, partly through inhibition of proliferation activity caused by serum growth factors. Furthermore, they indicate that certain flavonoids may be useful for prevention of colon carcinogenesis in obese humans.

Topics: Animals; Antioxidants; Azoxymethane; Carcinogens; Colonic Neoplasms; Dietary Supplements; Flavones; Flavonoids; Insulin; Leptin; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Precancerous Conditions; Quercetin