HE435 Lecture Notes - Lecture 7: Adipose Tissue, Adipocyte, Thermodynamics
Document Summary
Etiological considerations: adipose tissue is an endocrine organ, meaning what, obesity is the result of a chronic imbalance between energy intake and energy expenditure. Pathophysiology: three key hypotheses to consider, lipid overflow hypothesis, adipokine hypothesis. Similar mechanism of action: likely that the effects of each contribute, one hypothesis cannot sufficiently explain obesity. Adipokine hypothesis: very similar to the inflammation hypothesis , adipose tissue secretes cytokines, cytokines exert effects locally or on other tissues, adiponectin (regulation of glucose & fat metabolism, leptin. Lipid overflow hypothesis: adipose tissue has a maximum storage capacity. Inflammation hypothesis: adipocyte hypertrophy leads to low po2, hypoxia, and increased production of. Ros: resulting in il-6 and tnf- secretion, these adipokines spillover into the circulation leading to the pro-inflammatory state in the characterizes obesity. Tissue specific metabolic consequences: skeletal, disrupted, fas, tags, dags, acyl coas, ceramides, insulin sensitivity (ie. resistance, chronic low-grade inflammation. Inhibited: tnf- , il-1 , il-6, ffas nfkb pathway activation.
