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Hypertrophic obesity inhibits activation of peroxisome proliferators-activated receptor gamma (PPARγ), considered the key mediator of the fully differentiated and insulin sensitive adipocyte phenotype. We examined the effects of Caffeic Acid Phenethyl Ester (Cape), isolated from propolis, a honeybee hive product, on Adipose Stem Cells (ASCs) differentiation to the adipocyte lineage. Finally we tested the effects of Cape on insulin-resistant adipocytes. Quantification of Oil Red O-stained cells showed that lipid droplets decreased following Cape treatment as well as radical oxygen species formation. Additionally, exposure of ASC to high glucose levels decreased adiponectin and increased proinflammatory cytokines mRNA levels, which were reversed by Cape-mediated increase of insulin sensitivity. Cape treatment resulted in decreased triglycerides synthesis and increased beta-oxidation. Exposure of ASCs to Lipopolysaccharide (LPS) induced a reduction of PPARγ, an increase of IL-6 levels associated with a well-known stimulation of lipolysis; Cape partially attenuated the LPS-mediated effects. These observations reveal the main role of PPARγ in the adipocyte function and during ASC differentiation. As there is now substantial interest in functional food and nutraceutical products, the observed therapeutic value of Cape in insulin-resistance related diseases should be taken into consideration.

Coronary heart disease is the main cause of death in postmenopausal women (PMW); moreover its mortality exceeds those for breast cancer in women at all ages. Type II diabetes mellitus is a major cardiovascular risk factor and there is some evidence that the risk conferred by diabetes is greater in women than in men. It was established that the deficiency of endogenous estrogens promotes the atherosclerosis process. However, the impact of estrogen replacement therapy (ERT) on cardiovascular prevention remains controversial. Some authors strongly recommend it, whereas others revealed a concerning trend toward harm. This review tries to underlines the different components of cardiovascular risk in diabetic PMW and to define the place of ERT.