Term
| List the reactants and products involved in triacylglycerol (TAG) synthesis. |
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Definition
TAG synthesis in liver and adipose tissue
exits liver as VLDL
DHAP(liver/adipocyte-NADH OBLIGATORY) or Glycerol(LIVER ONLY-ATP) = Glycerol-3-P + 2 Fatty acyl CoA's = Phosphatidic acid
(alt pathway can branch here to form phosphoglyceride)
Phosphatidic acid - Pi = Diacylglycerol + Fatty acyl CoA = TAG
Dihydroxyacetone phosphate (DHAP) - major biochemical role is in the glycolysis metabolic pathway (aka:glycerone phosphate in older texts) |
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Term
| Describe basic hormone action on adipose formation and breakdown (aka adipose cycle). |
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Definition
Insulin stimulates TAG synthesis, while glucagon/stress hormones stimulate its breakdown
Fed state/high insulin
lipase phosphatase kills hormone-sensitive lipase anabolic state
Fasted state/high glucagon
PKA activates hormone sensitive lipase
catabolic state, lipolysis-adipose FA's into blood |
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Term
| List the key enzymes involved in TAG synthesis. |
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Definition
Fatty acid synthase (liver)
MAKES fatty acyl-CoA
Glycerol kinase (liver)
glycerol to glycerol-3-P (NEEDS ATP-product forms TAG)
Lipoprotein lipase (adipose, muscle)
BREAKS fatty acids off of circulating VLDL
Phosphatidate phosphohydrolase
BREAKS off Pi - MAKES Diacylglycerol (product into TAG) |
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Term
Adipose tissue is an endocrine organ. Endocrine organs secrete stuff.
Tell me what secretions adipose tissue secretes and what does those secretions do? |
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Definition
Leptin
"Enough fat" signal, slows roll at hypothalamus
-leptin deficiency/resistance asscoiated with obesity
Adiponectin
modulates glucose metabolism and fatty acid catabolism - decreased in CHD patients
Fatty acids
Insulin resistant adipocytes secrete FA's in an unregulated fashion
AGE, PAI-1
coagulation factors
IL-6, TNFalpha, ASP, Resistin
cytokines: influence arteriole surface conditions, can result in irritation and subsequent atherosclerosis |
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Term
| How can lipolysis lead to hyperglycemia? |
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Definition
Adipocytes: Up lipolysis = Up FFA mobilization
Muscle: Up FFA oxidation, resulting in less glucose utilization
Liver: Up FFA oxidation = Up gluconeogenesis
Net result: more circulating blood glucose/hyperglycemia
This mechanism is associated with insulin resistance diabetes pathology |
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Term
| List typical pathological findings of four tissue types in patients with Type II 'beetes. |
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Definition
Adipose: increased nonesterified fatty acids (free FA's)
Muscle: decreased glucose disposal
Hepatic: increased gluconeogeneis and glucose output
Endothelial: dysfunctional - associated with arterial damage (TII diabetics have predisposition to CHD) |
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Term
| What are three metabolic actions and potentially deleterious consequences of high levels of free fatty acids can have on the liver? |
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Definition
1. Up's glucose production (hyperglycemia)
2. Up's lipid synthesis (high TAG levels/fatty liver)
3. Up's secretion of prothrombotic proteins (clots, CHD exacerbation) |
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Term
| What are the risk factors for CHD in a diabetic patient? |
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Definition
[image]
Also Up'd FFA and VLDL |
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Term
| List five of the constellation of interrelated disorders associated with Metabolic Syndrome. |
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Definition
Abdominal obesity
Up'd TG's and low HDL-C (atherogenic dyslipidemia)
Up'd BP
Insulin resistance, With or W/o glucose intolerance
Prothrombotic/proinflammatory markers
(Up'd CRP, fibrinogen, and other coagulation factors) |
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