Starvation and Metabolic Syndrome Flashcards
What combination of hormones leads to the largest rise in blood glucose?
- glucagon, epinephrine, and cortisol.
- synergistic effect.
Main hormonal activators of glycogenolysis:
- norepinephrine and epinephrine.
- glucagon too, but not as strongly.
Main hormonal activators of gluconeogenesis:
- cortisol and glucagon.
- norepi/epi do not trigger gluconeogenesis.
What hormone stimulates both liver glycogenolysis and gluconeogenesis?
glucagon.
The 4 types of hypoglycemia:
- Insulin induced.
- Postprandial.
- Fasting.
- Alcohol.
Treatment for mild and severe insulin induced hypoglycemia:
- mild: oral carbohydrates.
- severe: glucagon shot.
Main glucose sources during starvation (time 0 to weeks):
- ingested glucose (4 hours).
- glycogen stores (4-18 hours).
- gluconeogenesis.
Once liver glycogen stores are depleted in starvation, what two important changes in body metabolism occur?
- gluconeogenesis in liver and kidneys increases.
- fatty acids/ketones become primary metabolic fuel; spares glucose for brain and RBCs.
When do ketone bodies become the primary source of metabolic fuel?
14-21 days of starvation.
What is the primary ketone body produced during starvation?
- beta-hydroxybutyrate.
- results from NADH and acetyl CoA produced by FA beta-oxidation.
Brain fuel source during fed state:
100% glucose.
Brain fuel source during starvation state:
- 60% beta-hydroxybutyrate.
- 30% glucose.
- 10% acetoacetate.
Metabolic syndrome is defined as meeting three or more of the following criteria (5):
- central obesity
- high fasting triglycerides
- low HDL
- hypertension
- hyperglycemia
Which two types of fat are insulin sensitive and aid in maintaining/lowering blood glucose?
- Brown fat.
- Subcutaneous white fat.
Which type of fat is insulin resistant?
visceral white fat.
What three things does visceral fat secrete in excess, which promote dyslipidemia, insulin resistance and inflammation?
- inflammatory markers (C-reactive protein).
- free fatty acids.
- adipokines (cytokines).
What is hypothesized to be the main cause of T2 diabetes due to visceral fat/metabolic syndrome?
increased FFA secretion from visceral fat.
Effects of increased FFA secretion from visceral fat on metabolism:
- inhibits insulin secretion.
- decrease glucose uptake in muscle and adipose tissue (insulin activates GLUT4).
- increase gluconeogenesis (increase glucagon/insulin ratio by lowering insulin).
HYPERGLYCEMIA / T2 DIABETES
The three hormones secreted from adipocytes affecting blood glucose (and their classification):
- Resistin (pro-hyperglycemic).
- Leptin (anti-hyperglycemic).
- Adiponectin (anti-hyperglycemic).
The main downstream molecule of resistin, leptin, and adiponectin is:
AMPK
How does resistin released from adipocytes promote hyperglycemia?
- resistin inhibits AMPK and activates gluconeogenesis.
- AMPK promotes glucose uptake (GLUT4) and glycolysis.
How do leptin and adiponectin released from adipocytes promote glucose uptake?
- leptin and adiponectin activate AMPK.
- AMPK promotes glucose uptake (GLUT4) and glycolysis.
What changes in adiponectin, leptin, and resistin will cause obesity?
- adiponectin and leptin deficiency.
- adiponectin and leptin receptor defects.
- resistin levels are high.
What hormone released from adipocytes interacts with the CNS, and how?
- leptin; reduces food intake and increases energy expenditure via hypothalamus.
