Topic 2, L1 & 2 - Nutrition, Metabolism and Energy Balance II Flashcards
(47 cards)
Hypoglycemia
Low blood sugar
- Since the brain needs glucose to function, can go into coma (not enough fuel)
Increase in blood glucose levels above homeostatic range …
Sensed by pancreas → Releases insulin to stim absorption of glucose from blood by liver / excess glucose can also be stored as glycogen → Glucose also absorbed by tissue cells for their use to produce energy → Some glucose will be taken up by fat cells, stored as triglycerides
(all occurs in the absorptive state)
[ net effect = fall in glucose ]
Decrease in blood glucose levels below homeostatic range …
Sensed by pancreas → Releases glucagon to tell body to tap into glucose reserves (glycogen) that were stored during the absorptive state to break them down & release that glucose back into the blood stream
[ net effect = rise in glucose ]
Overview of the Pancreas
Triangular gland located partially behind stomach with both exocrine & endocrine cells
- Acinar cells (exocrine) produce enzyme-rich juice for digestion
-
Pancreatic islet cells (islets of Langerhans) contain endocrine cells
- Alpha (α) cells produce glucagon (hyperglycemic hormone – raises blood glucose levels)
- Beta (β) cells produce insulin (hypoglycemic hormone – lowers blood glucose levels)
- Delta (D) cells secrete somatostatin(suppresses release of both glucagon & insulin, slows rate of food absorption / energy secretion along GI tract)
- F cells produce pancreatic polypeptide [ PP ] (inhibits gallbladder contraction, regulates production of pancreatic enzymes)
How & when is insulin secreted ?
Insulin is synthesized as proinsulin, which is then modified. It will be secreted in the case when :
- Blood glucose levels increase / exceed normal range
- Blood levels of amino acids and fatty acids increase
- ACh is released by parasympathetic nerve fibers
What are the effects of insulin on metabolism?
- Accelerates glucose uptake / absorption (all target cells)
- Stimulates glycogen formation (skeletal muscle fibers, liver cells)
- Stimulating amino acid absorption & protein synthesis (all target cells)
- Stimulates ffa absorption & triglyceride formation (adipocytes)
So, its net effects are :
↓ Blood glucose / ↑ Glycogen storage
↓ Blood amino acids & FFA (fatty acids)
3 ways Insulin lowers blood glucose levels
- Enhances membrane transport of glucose into fat + muscle cells
- Inhibits breakdown of glycogen to glucose
- Inhibits conversion of amino acids or fats to glucose
How & when is glucagon secreted ?
Glucagon is a potent hyperglycemic agent, and its secretion is triggered by :
- Decreased blood glucose levels
- Rising amino acid levels
- Sympathetic NS
What are the effects of glucagon on metabolism?
- Stimulates breakdown of glycogen (skeletal Muscle Fibers & liver Cells)
- Stimulating breakdown of triglycerides (adipocytes / fat cells)
- Stimulates production & release of glucose (liver cells)
So, net effects are :
↑ Blood glucose / ↓ glycogen storage
↑ Blood amino acids & FFA
3 ways Glucagon raises blood glucose levels
Targets liver to :
1. Break down glycogen into glucose
2. Synthesize glucose from lactic acid and other noncarbohydrates
3. Release glucose into blood
Whether glucose is absorbed by the digestive tract or manufactured and released by the liver, ____________________________________________________
very little glucose leaves the body once it has entered the bloodstream
Diabetes Mellitus (DM)
Group of metabolic diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both
- Complex disorders of CHO, fat and protein metabolism
DM & Kidneys
The kidneys reabsorb virtually all glucose, so glucose does not appear in the urine. However, in diabetes mellitus, glucose accumulates in the blood and urine as a result of faulty glucose metabolism
Type 1 DM
Autoimmune destruction of pancreatic β-cell (insulin producing cells) which causes absolute insulin deficiency since beta cells are the sole insulin producing source in the body
Results from hyposecretion OR hypoactivity of insulin (insulin is ABSENT)
- Requires daily insulin injections / can be multiple times a day
if there is NO INSULIN = Cannot pull glucose from bloodstream into ECF into cell bc there is no insulin signal
Type 2 DM
More common
- Produces normal amounts of insulin initially but their tissues don’t repond efficiently – insulin resistance_
Insulin is PRESENT, but its effects are deficient
- Causes an interference with insulin binding to target tissue [ we can have receptor + hormone + everything we need, but it binds but does nothing else (put key into lock, but not unlock, glucose cannot move into system) ]
Treatment : Non-insulin type therapies, oral hypoglycemics
In either case of DM, blood glucose levels remain _____ after a meal because glucose is _____________________________________.
high, unable to enter most tissue cells
What is the function of glucose transport proteins ?
Facilitate movement of glucose into cells
Insulin binds to its receptor → Initiates signal transduction cascade → Tells vesicles to move from within cytoplasm of cell via exocytosis & insert transporters into plasma membrane to allow glucose to move into the cell via
What happens in the absence of insulin ?
If we have no insulin, we may still have all components needed for transport pathway → BUT nothing that tells glucose transporters to insert into cell membrane
Transport proteins are not embedded in plasma membrane of target cell (actually in secretory vesicles within cell tself) → USELESS (we need to get them to move from out of the cell into plasma membrane)
What are the consequences of insulin deficiency ?
Effects on liver, skeletal muscle, adipose tissue
[ see table ]
- Polyuria. Excessive glucose in the blood leads to excessive glucose in the kidney filtrate where it acts as an osmotic diuretic (that is, it inhibits water reabsorption by the kidney tubules). The end result is polyuria, a huge urine output that
decreases blood volume and causes dehydration. - Polydipsia. Dehydration stimulates hypothalamic thirst centers, causing polydipsia, or excessive thirst.
*
Polyphagia. Polyphagia refers to excessive hunger and food consumption, a sign that the person is “starving in the land of plenty.” Although plenty of glucose is available, the body cannot use it. Instead, the body breaks down protein and fat to supply energy, and this is thought to stimulate appetite.
When sugars cannot be used as cellular fuel, more fats are mobilized, resulting in high fatty acid levels in the blood, a condition called lipidemia. In severe cases of diabetes mellitus, blood levels of fatty acids and their metabolites (acetoacetic acid, acetone, and others) rise dramatically. The fatty acid metabolites, collectively called ketones (ke’tonz) or ketone bodies, are organic acids. When they accumulate in the blood, the blood pH drops, resulting in ketoacidosis, and ketone bod-
ies begin to spill into the urine (ketonuria).
Severe ketoacidosis is life threatening. The nervous system
responds by initiating rapid deep breathing (hyperpnea) to blow offcarbon dioxide frorn the blood and increase blood pH. (We will explain the physiological basis of this mechanism in Chapter 22.) Serious electrolyte losses also occur as the body rids itself of excess ketone bodies. Ketone bodies are negatively charged and carry positive ions out with them, so sodium an
abdominal pain and possibly vomiting. If untreated, ketoaci- dosis disrupts heart activity and oxygen transport, and severe depression of the nervous system leads to coma and death.
The opposite condition to diabetes mellitus is hyperinsulin- isn,, or excessive insulin secretion. It causes low blood glucose
levels, or hypoglycemia.This condition triggers the release of hyperglycemic hormones, which cause anxiety, nervous- ness, tremors, and weakness. Insufficient glucose delivery to the brain causes disorientation, progressing to convulsions, unconsciousness, and even death. In rare cases, hyperinsu- linism results from an islet cell tumor. More commonly, it is caused by an overdose of insulin and is easily treated by ingesting sugar.
Gluconeogenesis
Production / synthesis of glucose from non-carbohydrate sources (non-sugar substrates)
Glycogenolysis
What are the metabolic consequences of Type 1 DM ?
When sugars cannot be used as fuel, as in DM, fats are used, causing lipidemia (high levels of fatty acids in blood)
Fatty acid metabolism (lipolysis) results in formation of ketones (ketone bodies)
- Ketones are byproducts of betaoxidation (there is so much acetyl-CoA floating around → overwhelms citric acid cycle, so converted into temp storage)
- As they are acidic, their build-up in blood can cause ketoacidosis, as well as ketonuria (their presence in urine, which can cause pulling of cations with them)
Untreated ketoacidosis causes hyperpnea, disrupted heart activity and O2 transport, & severe depression of the NS that can possibly lead to coma and death [ Mainly consequence of TYPE 1 DM, in type 2, we have some insulin around that is usually enough to prevent ]
What is the opposite condition to diabetes mellitus ?
Hyperinsulinism – Excessive insulin secretion causing low blood glucose levels ( hypoglycemia )
- Symptoms include anxiety, nervousness, disorientation, unconsciousness, even DEATH
- Treatment : Sugar ingestion
What are the risk factors for Type 2 DM ?
Age, obesity, hypertension, physical inactivity, pregnancy & family history
