1. Dietary fructose can specifically increase hepatic de novo lipogenesis (DNL), promote dyslipidemia, decreases insulin sensitivity, and increase visceral adiposity in overweight/obese adults.
2. Fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome.
3. Dietary fructose can reduce circulating insulin and leptin, attenuate postprandial suppression of ghrelin, and increase triglycerides in women.
4. Fructose is transported into neocortical cells, including nerve terminals, and that it is metabolized and thereby detoxified primarily through hexokinase activity.
1. Progesterone (P4) maintains uterine quiescence in pregnancy, and a proposed functional withdrawal of P4 classically regulated by nuclear Progesterone receptors (nPRs) leads to labor, P4 can affect the functions of macrophages despite the reported lack of expression of nPRs in these immune cells.
2. Stimulation of breast cell tumorigenesis and tumor growth accompanying Progesterone treatment is due to the Progesterone metabolite 5αP, and that breast tumorigenesis can be blocked with the 5α-reductase inhibitor, finasteride.
3. Exogenous Progesterone increases Nuchal translucency, NT seen ultrasonographically at 11-14 weeks' gestation is a sensitive marker for Down syndrome.
4. Progesterone decreases the rate of lipolysis in the inguinal WAT of female rats, inhibiting the activity of both ATGL (by stimulating synthesis of G0S2 - specific inhibitor of the enzyme) and HSL.
1. Estrone , a steroid known to play an important role as precursor of 17 beta-estradiol , especially in postmenopausal women.
2. Estrone and 17beta-estradiol can increase the cellular accumulation of topotecan in K562 / BCRP cells, but not in K562 cells, suggesting that these estrogens inhibit the BCRP-mediated drug efflux and overcome drug resistance.
3. The widely distributed estrone esters in food and their relatively high concentrations may result in high free hormone intakes in humans, the continued and massive intake of estrone may enhance tissue deposition and lead to obesity.
1. Dodoviscin H can promote adipocyte differentiation as characterized by increased triglyceride levels in 3T3L1 cells.
1. Dodoviscin I can promote adipocyte differentiation as characterized by increased triglyceride levels in 3T3L1 cells.