Starvation Flashcards
What are some lifelong impacts of malnutrition?
Increased vulnerability to disease, developmental delays, stunted growth, and blindness.
Malnutrition
often associated with starvation , but can have a specific nutritional deficiency or excess
Starvation
in elderly that don’t receive nutrition, chronically ill patients, and those affected by trauma or infection
What are the metabolic functions of liver in fed state?
uptakes glucose via GLUT 2 and converts excess glucose to glycogen. It also produces Acetyl CoA for TG storage via VLDL that goes into circulation, and synthesizes proteins from excess AAs.
What do other tissues outside of the liver do during the fed state?
Glucose is main source of energy so adipose stores TGs, brain uses glucose, RBCs use glucose, and muscles take up via GLUT4, stores as excess glycogen or makes proteins from excess AA.
How is blood glucose maintained in the Basal/ Post Absorptive state?
Blood glucose peaks 1hr after a meal and returns to fasting 2hrs later. After, liver maintains glucose through glycogenolysis until depleted. After depletion, liver does gluconeogenesis via lactate, glycerol, AA. FA are main fuel source. Muscles use glycogen, FA, KB. Brain and RBCs use glucose.
What are liver, muscle, adipose, brain, RBCs, and kidney using as energy during prolonged fasting?
Liver is barely doing gluconeogenesis by making fatty acids into ketone bodies. Muscle decreases its use of glucose and increases use of FAs. Uses KBs for a brief moment, but begins decreasing AA so liver can do gluconeogenesis for brain. This decreases urea production, Adipose continues making FAs and glycerol. Brain begins using more KBs (exclusively KB after 2 weeks). RBCs use glucose for anaerobic glycolysis. Kidney secretes less urine.
What decreases compared to fasting for 24 hrs to prolonged fasting?
urea production, muscle degradation, liver gluconeogenesis, brain use of glucose, and muscle use of ketone bodies all decrease
which tissues can perform beta oxidation?
Liver, kidney, muscle
which tissues can form KBs?
Liver and kidney
which tissues can perform lipogenesis?
liver and adipose
Nitrogen equilibrium vs. positive balance vs. negative balance
Equilibrium is when nitrogen intake = excretion, positive balance = nitrogen intake > excretion, and negative balance = nitrogen intake < excretion (starvation, trauma, cancer)
Pathological adaption
Metabolic changes to restore nitrogen equilibrium at expense of some lean tissue
Minimum protein requirement
Amount of protein in person’s diet below which they cannot re-establish a nitrogen balance with normal diet
What’s immediate response to starvation?
proteolysis of skeletal muscle to increase AA catabolism
What’s prolonged starvation response?
low insulin increases muscle proteolysis to maintain nitrogen. This large loss of muscle and urea is adapted to after a few days and you lose less muscle because the goal of starvation is to reduce free AAs
How do you die from starvation and what are determining factors?
you die when you lose about 40% of your body weight. Factors determining survival are starting adipose tissue levels, protein levels, vitamin/mineral precursors, and electrolyte composition.
Diabetes Mellitus
Metabolic disorder characterized by an elevated fasting blood glucose caused by a relative or absolute deficiency in insulin.
Type 1 diabetes
hyperglycemia, an absolute deficiency in insulin caused by an autoimmune attack against the beta pancreatic cells
Type 2 diabetes
hyperglycemia due to insulin resistance, impaired insulin secretion, and dysfunctional beta cells
What’s happening in metabolism of patient with diabetes?
There’s impaired glucose uptake because tissues can’t use it. Liver increases glycogenolysis, increases gluconeogenesis by making FAs into KBs. Adipose increases mobilization of TGs for lipolysis to release FFAs to liver. Muscle increases glycogenolysis and gluconeogenic precursors. Kidney makes KBs.
Cachexia
metabolic syndrome associated with chronic diseases like kidney disease, pulmonary disease, advanced cancer, AIDs. Characterized by decreased skeletal muscle without fat mass loss. This is caused by release of pro-inflammatories like TNFa, Il-1, Il-6, and IFNy that activate ubiquitin pathway.
What are clinical presentations of cachexia?
weight loss, fatigue, decreased skeletal muscle, anemia, atrophic diaphragm, increased hepatic protein synthesis
Anorexia nervosa
Self starvation. Clinical presentations: dehydration, electrolyte imbalance, low LSH, low thyroid hormone (cold), constipation, dry skin, osteoporosis, anemia, and hypalbuminemia
