Term
| ___ is fastest growing disease in America. |
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Definition
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Term
| components of energy expenditure: |
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Definition
- basal metabolism
- adaptive thermogenesis
- physical activity |
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Term
| Pima Indians that live in the U.S. : |
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Definition
50% have type 2 diabetes
75% are overweight or obese |
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Term
| Pima Indians that live in central america: |
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Definition
few are obese
few have diabetes |
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Term
| Leptin and adipnectin are good. PAI-1, AGE, IL-6, TNFa, ASP, and resistin are bad. |
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Definition
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Term
| three areas of the brain involved with eating: |
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Definition
- cortex
- limbic areas
- hypothalamus |
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Term
| what role to the cortex and limbic areas play in eating? |
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Definition
| - cognitive and reward control of feeding |
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Term
| what role does the hypothalamus play with eating? |
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Definition
- homeostatic control of eating
- energy expenditure
- hormones |
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Term
| With increasing BMI, there is a ___ in the clearance of glucose from the blood. |
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Definition
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Term
| Insulin resistance is a multisystem disorder. Explain how it affects adipose tissue, muscle, liver, endothelium. |
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Definition
- adipose tissue: increased NEFA and adipokine release
- muscle- decreased glucose disposal
- liver- increased gluconeogenesis and hepatic glucose output
- endothelium- endothelial dysfunction |
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Term
| what is a major contributor to insulin resistance? |
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Definition
- abdominal obesity
- overabundance of circulating fatty acids |
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Term
| abdominal obesity leads to: |
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Definition
- Increases fatty acids in systemic circulation
- Intra-abdominal obesity increases the flux of adipose tissue-derived free fatty acids to the liver. In the liver, fatty acids exert direct effects on:
Glucose production
Lipid synthesis
Secretion of prothrombotic proteins |
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Term
| how does abdominal obesity lead to insulin resistance? |
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Definition
- IL-6, TNF-a, cytokines result in inflammation
- ultimately the insulin receptor IRS1 and 2 won't work |
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Term
| location (visceral fat) has been demonstrated to have important metabolic consequences. One of these consequences is the release of free fatty acids in the blood stream, which is directly responsible for insulin resistance. In addition, overloaded adipocytes also produce various cytokines involved in subclinical inflammatory process and oxidative stress. An important effect of these adipocytokines is the alteration of insuline receptor sbustrate which is also involved in the insulin resistance process. |
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Definition
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Term
| explain how someone gets T2DM? |
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Definition
- genetic defects so that beta cells don't secrete insulin as they should
- obesity> insulin resistance so inadequat use of glucose
- hyperglycemia
- beta cell exhaustion
- T2DM |
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Term
| fasting blood glucose must be above: |
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Definition
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Term
| pathophysiology defects with T2DM: |
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Definition
- increased glucagon from alpha cells
- decreased insulin from beta cells
- hyperglycemia
- insulin resistance
- decreased glucose uptake by muscle and fat |
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Term
| rare inherited mutations that might lead to insulin resistance: |
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Definition
- insulin receptor
- glucose transporter
- signaling proteins |
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Term
| results of metabolic syndrome: |
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Definition
- reduced glucose tolerance
- hyperinsulinemia
- hypertension
- visceral obesity
- hemostatic disorders
- elevated TG
- normal or slightly elevated LDL
- HDL diminished |
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