Exam 7 Flashcards
What are the actions of insulin?
STOPS:
- Gluconeogenesis
- Glycogenolysis
- Lipolysis
- Ketogenesis
- Proteolysis
Go:
-Glucose uptake in muscle
-Glycolysis
-Glycogen synthesis
-Protein Synthesis
Uptake of Ions specially K+, PO4
How does Insulin affect carbohydrates metabolism?
Decrease blood glucose by helping glucose leave blood and limiting the raise in blood glucose
Increases glucose transport and adipose into muscle
Promotes gycogen formation in liver and muscle
Aids GLUCOKINASE: phosphorylation of glucose
Inhibits gluconeogenesis and glycogenolysis
Actions of Insulin in Lipids metabolism
Overall, Inhibits mobilization and oxidation of FA
Inhibits Ketogenesis
Ketogenesis: breakdown of FA in liver, during fasting produces Ketoacidosis.
Promotes FFA storage as Triglycerides. LIPOPROTEIN LIPASE-Storage of triglycerides
Inhibits uptake of FFA in muscles, in favor of glucose uptake in muscles
Inhibits Lipolysis: HORMONE SENSITIVE LIPASE
The effects of protein are overall cataolic or anarobic?
ANABOLIC
Decreases blood AA
Increases AA and protein uptake by tissues
Increases protein synthesis
Inhibits protein degradation
What are the other actions of insulin?
Increases activity of Na/K ATPase pump = Uptake of K+ into cells
Promotes Phosphate, Mg++ uptake into cells
Decreases appatite via the SATIETY CENTER in HYPOTHALAMUS
What happens when there is an excess of insulin in the blood/body?
Causes HYPOGLACEMIA
Cortisol release is stimulated to increase appetite
What or how does Insulin Resistance occur?
When blood insulin remains high (over-produced) and the cells fail to respond normally. This is a defensive mechanism during illness to protect brain’s glucose supply.
Resistance can occur due to receptors alterations, decreased affinity or number of receptors.
Post-receptor changes in the intracellular action of insulin.
How do Hormones cause insulin resistance?
Cortisol, GH, Thyroid hormones, Epinephrine, Estrogen/Progesterone:
Epi: antagonizes insulin and stimulates the release of glucagon, thus increasing blood glucose
Progesterone: during pregnancy favors the transfer of nutrients to fetus.
How does obesity cause insulin resistance?
Type II diabetes
Impared insulin signaling
Decrease GLUT4 expression in adipose and muscle tissue or it can be normal, but Decrease Transport of clucose occurs due to TRANSLOCATION/DOCKING of GLUT4 into plasma membrane.
How does liver or kidney failure cause insulin resistance?
Sepsis and Insulin Antibodies?
Defect in kidney results in defect of Post reception pathway and possible decrease in GLUT4 in skeletal muscle.
Sepsis: Insulin signaling defect with infection. Stress causes hypoglacemia, release of glucose.
Insulin antibodies affect the normal effects of insulin
Characteristics of Diabetes Mellitus type 1 and type 2
Type 1: insulin defficiency due to destruction of pancreatic Beta cells, autoimmune issue usually
Type 2: Insulin resistance: can be associated with down-regulation of insulin receptors in muscle and adipose tissues or issues with insulin signaling.
What is Insulinoma?
Excessive production of insulin by Beta cells in the pancreas
What are the results of lack of insulin or lack of insulin action?
Hyperglacemia due to decrease in hepatic output: Type 2 diabetes and decreased glucose uptake by cells. Cell starvation
Increase in glycogenic AAs liver keeps making it
Increase glucagon release because carbohydrate ingestion does not suppress it
Blood Hyperosmolality: glucose draws water and doesn’t leave
Osmotic diuresis in kedney: beyond threshold ~300 mOsm/L, glucose excess in urine and water follows.
Hyperlipidemia: Increased oxydation of fat, Fat accumulation in liver, Increase Ketoacidosis.
Increase glycolysis and Increase Lipid uptake
Peripheral tissue catabolism: Muscle wasting and weight loss
Increase gluconeogenesis and Decrease AA uptake by cells
Glucagon
What cells secret it?
What stimulates its release?
What inhibits its release?
Secreted by alpha cells in the pancreas
Synthesized as preproglucagon untils its release
Sequence is identical in all species
Stimulation: Hypoglacemia, Protein, and AA intake/ingestion
Fasting, Stress (specially infection), Intense excercise, CCK (CHOLECYTOKININ is released when protein and fat is ingested)
Inhibition: Glucose, Insulin, SOMATOSTATIN
Actions of Glucagon
Pathophysiology
G-protein/cAMP
Opposite of Insulin actions
Mobilizes energy, Increases glycogenolysis, gluconeogenesis, lipolysis, ketoacid formation
Little to no effect on glucose utilization by peripheral tissues.
Pathophysiology
Tumor of Alpha cells Glucagonoma
Results in Diabetes Mellitus and Necrolytic Migratory Erythma (blisters, swelling and pressure in areas of body)
Hyperglucagonemia/diabetes mellitus with infection
Glucagon:Insulin ratio increases
Where is Somatostatin secreted?
Delta cells of pancreas, Hypothalamus, and GI cells
SS-28: GI tract
SS-14: Pancreas and Hypothalamus
Stimulated by all nutrients
Inhibits Insulin, Glucagon, GI Hormones, GI motility, enzymes, gastric acid secretion.
AAs are needed for liver to perform gluconeogenesis
Adipose tissue as an Endocrine organ
Leptin and Adiponectin
Leptin
Inhibits appetite by inhibiting Neuropeptide Y
Increase BMR
Leptin resistance may contribute to Obesity
Adinonectin
Improves insulin sensitivity
High adinonectin = low risk of Type II diabetes
Low adinonectin = obesity and diabetes in cats by increasing TYROSINE PHOSPHORYLATION in insulin receptor in skeletal muscle
What are the processes and regulatory systems that depend on calcium and phosphorus?
Vitamin D
Parathyroid Hormone
Calcitonin
Neurotransmission, learning, memory, muscle contraction, mitosis, mobility, secretion, fertilization, blood clotting, structure of bones and teeth.
Intestine: absorbs
Kidney: Reabsorption
Skeleton: Reservoir
Skin: Makes it
Liver: Makes it
What is they biologically active form of calcium?
Where is the highest concentration?
What cells are involved in calcium homeostasis?
Highest: Extracellular
50% Ionidized (active) free form. The rest bound in albumin, complex anions.
10% complexed in other forms
Phosphate bicarbonate
Intracellular: lowest concentration
Cytosolic Ca++ can be increased as needed- fine balance control. Concentration depends on membrane permeability and motility. Intracellular storage.
The endocrine cell receptors are involved in Ca++ homeostasis
Endoplasmatic Reticulum: Calcium Channels, Na/Ca exchanger.
Hypercalcemia & Hypocalcemia
What causes alterations in the forms of Calcium in plasma?
Increase in plasma Ca concentration
Constipation, polyuria, polydipsia, lethargy, coma, death.
Hypocalcemia: decrease in plasma Ca++.
Twitching, cramping of skeletal muscle. Seizures, sensory and motor neurons highly excitable due to Lower threshold for excitation. Lower ECF Ca++
Numbness/tingling (paresthesia) seizures.
- Changes in plasma protein concentration
- Changes in complex anion concentration
- Acid-base disturbances
- Changes in HCO3 cuases changes in Calcium
- Lactation, Renal failure, Vitamin D disorders.
Acedemia and Alkalemia
What is the difference in Albumin-bound-calcium in each state?
Acedemia: More H in the blood
- High concentration of Ionized Ca++ (free form), so less is bound to Albumin
Alkalemia: Less H in the blood
-Low concentration of Ionized Ca++ bound to Albumin.
Calcium Homeostesis
What role do kidneys, intestines, parathyroid, and vitamin D have on this?
Bone is constantly remodeled to that Ca can be released into the blood or absorbed from blood.
Intestine absorbs Ca, the amount is regulated by Vitamin D.
Kidneys reabsorbed Ca and this is regulated by the PTH calcitonin
Calcitonin
Calcitonin works to control calcium and potassium levels. It does this by inhibiting the activity of the osteoclasts, the cells that break down bone. When the osteoclasts break down bone tissue, the calcium enters the bloodstream.
Osteoclast: bone reabsorbing cells Clast:collapsing
Osteoblast: bone forming cells Blast: building
Phosphate metabolism
Components of ATP, DNA, Lipids, Cofactors, RNA, bone
It regulated through urinary secretion
It is stored in Muscle
The percentage absorbed from diet is fairly constant
Balances many Cations and it is important for buffering and Magnesium absorption.









































































