In this review, we describe our current understanding of the molecular actions of estrogen and progesterone and their contributions to cellular metabolism, obesity, inflammation, and postmenopausal breast cancer.
Particular attention will be focused on the role of insulin resistance and recent advances in our understanding of the basic cellular mechanisms linking obesity and insulin resistance.
When he stumbled on this new cellular link between obesity and the immune system, immunologist Yair Reisner of the Weizmann Institute of Science in Rehovot, Israel, was studying something completely different: autoimmune diseases.
Hence, there is currently a critical requirement to understand the systematic and cellular mechanisms whereby obesity may both elicit MI and yet in some cases protect from subsequent events.
Here, we show that the protein Deleted in Breast Cancer-1 (DBC1) regulates cellular senescence during obesity.
It was proposed that cellular senescence during obesity and aging drives inflammation and dysfunction.
For example, Claussnitzer et al. examined the effects of CRISPR-Cas9-mediated editing on cellular signatures of obesity.
To begin to address these hypotheses, relevant findings about aging, obesity, cellular senescence, and inflammation in fat tissue will be considered.
To gain further insight into the molecular and cellular mechanisms of obesity in BBS animals, we examined the expression levels of key hypothalamic genes involved in leptin action.
Growing evidence indicates that the cellular stress linking obesity and increased circulating and subcellular markers of IR implies a crucial role of the endoplasmic reticulum (ER) stress response [ 15– 22].
