Adipose Tissue as Endocrine Organ Flashcards
Where do most of the FFAs in VLDL come from?
from the DIET, not de novo synthesized FFAs
Why are fatty acids transported with transport proteins and intracellular chaperones?
While the mechanism is not well understood for FA transport, we do know that TGs, **unoxidized FFSandsaturated CoA** are bad and can cause mitochondrial damage, cell damage, and apoptosis.
Cells also minimize this toxicity by converting FFAs to TAGs
percentage of adipocytes in adipose tissue and importance
only 20%
also capillaries, endothelial cells
mature adipocytes can get bigger or small depending on how much TGs are stored
White adipose makes several factors and contains enzymes that can activate/inactivate hormones. List the 7. All are secreted in proportion to the amount of adipose tissue except?
- Angiotensinogen PAI-1
- TNF-alpha, IL6, complement factors (pro-inflammatory)
- Aromatase (converts androstenedione and testosterone to estrone and estradiol)
- aP2 (stimulates hepatic GNG)
- 11-beta HD-1 (converts cortisone to cortisol)
- Leptin
- Adiponectin
Secretion of Adiponectin is inversely proportional to amount of adipose tissue
Main action of leptin
Think of leptin as stimulating growth, proliferation, reproduction, and energy use.
Leptin tells us theres enough energy on board. Reduces FFAs in cells to protect cells from lipid toxicity.
6 proposed roles of Leptin on intermediary metabolism
- reduces appetite, stimulates sympathetic regulation of metabolism – reduces efficiency of fuel use
- inhibits lipogenesis and promotes FFA oxidation in non-adipose tissues
- reduces hepatic VLDL secretion
- Decreases net TAG synthesis in adipocytes
- Increases glucose utilization in skeletal muscle - increases insulin sensitivity in this tissue
- Indirectly reduces hepatic GNG and glucose export
What are the two central targets of Leptin?
Pituitary and Hypothalamus
Specific effects of Leptin on Pituitary
(+) GH
(+) LH / FSH
(+) TSH
Specfic effects of leptin on hypothalamus
(-) food intake
(+) sympathetic output
(+) GnRH
(+) GHRH
Leptin has peripheral effects on these 5 targets
What is the action at each
- Pancreas: (-) insulin secretion
- Ovary: (+) steroid synthesis
- Blood vessels: (+) angiogenesis
- Thymus: (+) Thymopoiesis (CD4, CD8)
- Lymph Nodes: (+) T cells APCs
4-5 stimulates humoral and cell-mediated adaptive immunity, which is very energy consuming
An important thing large adipose tissue mass attracts
inflammatory cells! neutrophils and macrophages, which secrete pro-inflammatory molecules
2/3 of obese individuals are in a chronic inflammatory state: might contribute to insulin resistance and CVD
Adiponectin
- Secreted by adipocytes
- inversely proportional to fat mass
- Sensitizes target tissues to insulin and promotes pancreatic ß cell survival
- primarily secreted from visceral adipocytes
Which typye of fat is not desirable
Visceral adipose tissue . FFAs released from visceral fat (when insulin is low or in insulin resistance) are secreted into the hepatic portal system. Will accumulate in liver. Secreting VLDL, and now theyre competing with albumin bound FA for uptake by skeletal muscle and heart
Meanwhile, subcutaneous fats reach the vena cava and can be removed by skeletal muscle before liver encounters them.
Going to have dyslipidemia
Catecholamine sensitivity on subcutaneous vs. visceral fat
Visceral fat releases its FA much faster since its trigger by catecholamines. Thus considered more harmful
Insulin resistance, visceral fat, BMI
Insulin resistance follows visceral fat, but not BMI. Better to measure Waist: height ratio
