Prelim 2 Flashcards
(51 cards)
adipose tissue
largest endocrine organ that contains adipocytes, connective tissue, nerve tissue, and immune cells
- exists in a sac of collagen that allows for growth and shrinkage
types of mammalian fat
mechanical/behavioral fat and metabolic fat
stromal vascular compartment
cells of adipose tissue that are NOT adipocytes
subcutaneous fat
below the skin, different-sized adipocytes, metabolically active, vascularized
- leads to better adipogenesis
visceral fat
same-sized adipocytes, decreased lipolysis, increased triglyceride synthesis, less vascularization
What is some factors that control fat placement?
sex steroids and cortisol
estrogen
promotes subcutaneous fat accumulation
- reduces WAT fibrosis
- removing ovaries in mice = more visceral fat
2 ways adipose tissue can expand
hyperplasia and hypertrophy
hyperplasia
- fat stem cells become adipocytes through various steps
- uses PPARy
PPARy
a nuclear hormone receptor that is necessary for adipogenesis
- regulates lipid storage and insulin sensitivity
PPARy agonists for obesity
- they increase insulin sensitivity, stimulate adipogenesis, and improve glucose uptake
- they also led to heart attacks and strokes
hypertrophy
- adipocytes grow in size
- this can be normal (to an extent)
chronic adipocyte hypertrophy (CAH)
- leads to hypoxia, fibrosis, inflammation, and eventually, uncontrolled lipolysis
- more likely in visceral fat
hypoxia CAH
- happens due to increased intercapillary distance
- leads to cell death
- in ACUTE hypertrophy, new blood vessels can grow to accommodate
fibrosis CAH
1) initiation from hypertrophy and hypoxia
2) activation of fibroblasts
3) increased collagen and fiber deposition
4) full progression to organ failure
inflammation CAH
hypertrophic adipocytes secrete cytokines (like TNFa) that attract immune cells
- increased macrophage concentrations lead to adipocyte cell death
- insulin signaling pathways are impaired
adipocyte cell death
subcutaneous fat protects against adipocyte death, but visceral fat does not
TNF-alpha
pro-inflammatory adipokine that causes WAT inflammation
- increases in obesity and hypertrophy
- attracts macrophages
- anti-TNFa therapy in mice had NO effect on inflammation
types of macrophages in adipose tissue
M1: obese state
- promote cell death
- more prevalent in visceral fat
- recruit MORE M1 macrophages
M2: lean state
- angiogenesis and adipogenesis
- they become M1 in obesity
lipolysis
release of fatty acids
- turned on in the fasting state
- uncontrolled during insulin resistance b/c our body thinks we’re hungry
- uses HSL (hormone-sensitive lipase)
adipokines
hormones, peptides, or enzymes secreted from adipose tissue
- can have autocrine, paracrine, or endocrine signaling
leptin
an adipokine that tells us we’re full
1) secreted into blood from adipose tissue
2) activates leptin receptors on hypothalamus
3) up-regulation of gene transcription to curb appetite
leptin levels increase with fat mass
leptin therapy for obesity
had no effects on obese patients
- they can become resistant to leptin
lipodystrophy
partial to complete loss of adipose tissue
- leptin therapy can help