Control of blood sugar levels pogil. Glucose levels of the blood go hand in hand with insulin as one tries to regulate the other to maintain optimal body conditions and prevent terminal illnesses such as diabetes. We all understand the importance of glucose in our body but do you know that too much is poisonous? Well, controlling blood sugar levels pogil such as this sheds more light on what you need to know.
What keeps the body going?
How the body utilizes food is fundamental in understanding the pathology of diabetes, including how it affects the body. Typically, glucose and fat are the primary food components that fuel the body. Also, understanding how the digestive, intestinal and pancreatic hormones are involved in metabolism is helpful in the evaluation of diabetes problems and the normal functioning of the physiology.
The body cells use up glucose as a primary energy source. The blood plasma needs approximately between 60 and 100 mg/dl glucose concentration to maintain the normal body functions at an optimal level. When exercising or stressed, your body will require a higher glucose concentration, converted to energy for your muscles.
Through aerobic metabolism and the Krebs cycle, energy and water are produced courtesy of the glucose in the bloodstream. Alternatively, the body could use up fat and protein, but the breakdown of these components makes the body environment acidic, which isn’t optimal due to the production of ketoacids. Note that excessive amounts of ketoacids can cause metabolic acidosis.
Remember that there’s continuous absorption of glucose into the bloodstream due to the functioning of the body tissues. For ordinary non-diabetic people, there’s adequate replenishment of glucose levels in the bloodstream 10 minutes after a carbohydrate-oriented meal. The process continues even 2 hours after the carbohydrate meal.
With the second phase of insulin release at 20 minutes after the meal, the first phase begins 5 minutes later. Since the insulin effect’s duration is approximately 2 hours, taking a meal after 2 hours will show that the body utilized insulin well. Hours after the meal, the food is broken into various components, including glucose absorbed into the bloodstream through the intestines.
Glucose, being potential energy, isn’t utilized directly by the body. Instead, it is stored in the form of glycogen in the fat, muscles, and liver. Since the body is designed to survive, it stores energy in the fat. Most people who have excess fast replenish their glucose storage before the reserved energy in the fat is broken down and utilized.
The liver releases glycogen, i.e., stored glucose, to replenish the blood glucose when these levels fall after 2 hours. As a polysaccharide, glycogen s manufactured and stored in the liver cells. That way, glycogen can provide an energy reserve that can be dispatched for a sudden glucose deficit.
Poor Glucose Regulation
Diabetic individuals have persistent hyperglycemia. That is a sure sign of diabetes. People ailing from type 1 diabetes have body systems incapable of making little to no insulin. So, glucose stays in the plasma without the effects of insulin in lowering blood glucose levels.
The liver is also another contributor to chronic hyperglycemia. If a diabetic person is fasting, their liver will secrete excess glucose into the bloodstream. The secretion is bound to continue even after reaching optimal blood glucose levels. Also, skeletal muscles are a notable contributor to chronic hyperglycemia.
The muscles of a diabetic person take up little glucose after a meal which leaves the blood sugar levels high over longer periods. As for type 2 diabetic people, metabolic functioning of their skeletal muscles and their liver results in a combination of excess glucagon, beta cells dysfunction, decreased incretins, and insulin resistance.
During the early stages of the disease, insulin resistance can be counteracted by excessive insulin secretion from the pancreas’ beta cells that will try to put hyperglycemia in check.
Additionally, hyperglycemia caused due to insulin resistance is met by hyperinsulinemia, and then the beta cells begin failing. Once the excess insulin secretion can’t match hyperglycemia, the person will most likely develop clinical diabetes.
Endocrine hormones of the pancreas have a primary role in significant blood sugar regulation in which, through negative loop feedback, a discrete balance is maintained. Some of the pancreas’ hormones that affect glucose levels of the blood include; somatostatin, glucagon, amylin, and insulin.
Since the beta cells are formed at the beta cells of the pancreas, insulin is responsible for lowering blood sugar levels. On the other hand, glucagon, formed and secreted by the alpha cells, has a primary role in elevating blood glucose levels.
A strike in a balance between insulin and glucagon is initiated by the somatostatin hormone formed at the pancreas’ delta cells. In doing so, it alternates the turning on and off of each opposing hormone.
Since the ratio of secretion of amylin to insulin is regulated, it helps in elevating pancreas satiety to prevent overeating. Also, this phenomenon helps in emptying stomach content quickly to prevent the elevation of blood sugar levels.
Upon consuming a carbohydrate-oriented meal, digestion will trigger a rise in BG, which makes the pancreas turn off glucagon production and turn on insulin production.
Before activating the enzymes that convert glucose to glycogen, the liver cells will allow glucose from the bloodstream as long as both glucose and the insulin hormone remain plentiful. In this state, the liver will take from the bloodstream more glucose than it releases.
After meal digestion and the beginning of the fall of BG levels, glycogen synthesis will stop as insulin levels drop. If the body needs energy, glycogen is converted to glucose for easy transportation to the body cells through the bloodstream.
You should note that up to 10% of the total volume of a healthy liver is reserved for glucose storage. Also, only 1% of glucose is stored in the skeletal muscles. The liver regulates the glucose amount circulating between meals utilizing energy generated through the conversion of glycogen back to glucose.
Note that the liver can detect the amount of glucose to break down and release and the amount to store and keep. With that, it can maintain the ideal amount of glucose levels of the plasma. External management of the glucose levels is imitated by glucose therapy as a result of this process.
An ideal and optimal glucose concentration is in the levels of (60-100mg/dl). However, high concentration than the optimal levels can cause health problems as stated below;
At chronic levels, one can develop hyperglycemia -blood glucose concentration of more than 120mg/dl- which makes you susceptible to infection due to gradually tissue damage of the body. That way, your body sees the glucose as syrup in the bloodstream, which competes with life-giving oxygen and intoxicates the cells.
At acute levels, developing hyperglycemia – blood glucose concentration in the concentration greater than 300mg/dl – causes dehydration. On the other hand, concentrations of more than 500mg/dl cause profound hyperglycemia, leading to confusion, coma, cerebral edema, and eventually death.
Blood glucose concentration is determined by the rate of glucose leaving and entering the circulation. Glucagon and insulin hormones relay these signals throughout your body. Remember that optimal health requirements are as follows;
During high blood glucose concentration, the skeletal muscles and the liver eliminate glucose from circulation.
For low blood glucose concentration, your body is signaled into adding more glucose into the circulation.
Functions of glucagon
This is a peptide hormone secreted by the pancreas whose role is opposite to the effects of the hormone insulin, i.e., it lowers BG while insulin raises the BG levels.
Glucagon stimulates glycolysis upon reaching the liver, which breaks glycogen and glucose exportation into the circulation. Due to this occurrence, glucagon’s effects are considered catabolic, i.e., breaking down cells opposite to insulin’s anabolic effects. When there’s a significant drop in blood sugar levels, the pancreas releases the glucagon hormone.
Before release into the bloodstream, the glucagon hormone initiates the conversion of glycogen to glucose by the liver. Secretion of insulin is triggered if there’s a rise in BG. That way, the insulin allows the uptake and utilization of glucose by the body tissues dependent on insulin, e.g., muscles cells. Automatically, insulin and glucagon work together as a negative feedback system to stabilize the blood glucose levels.
Since glucagon is a potent blood glucose regulator, glucagon injections can be used in severe hyperglycemia correction. When glucose is taken parenterally or orally can elevate glucose levels of the plasma within a few minutes.
On the other hand, exogenous glucagon isn’t like glucose. An injection of glucagon can take between 10 and 20 minutes before muscle cell and bloodstream absorption and circulate to the liver, where there’s a trigger, breakdown, and glycogen storage. Notably, individuals with type 2 diabetes have glucagon secretin in excess in their bodies that are considered a high contributor of hyperglycemia of this type of diabetes.
With amylin secreted alongside insulin from the beta cells, this peptide hormone and insulin are released in the ratio of 1:100. Since it is essential to lower BG levels, amylin inhibits the secretion of glucagon. Amylin hormone depresses gastric emptying to reduce the abrupt increase in levels of the plasma BG after a meal.
Also, this hormone increases the brain’s satiety, i.e., it makes the brain detect when you’re full after a meal. That is why it is typically identified as the brain meal-connection hormone. The bodies of Individuals ailing from type 1 diabetes can’t produce inulin or amylin.
However, those with type 2 diabetes have adequate amylin amounts. So they seem to experience some difficulties with secretion hormones of the intestines (secretin), whose role is to regulate BG and satiety. That, in turn, causes these people to feel hungry. Note that various pharmaceutical analogs on this hormone have been created to curb complications arising from this hormone.
Role of insulin
Just as mentioned above, this is a peptide hormone manufactured in the beta cells of the pancreas whose primary role is to regulate the metabolism of the carbohydrates in the body. After any meal, this hormone is usually secreted in the bloodstream.
After reaching the insulin-sensitive cells in the liver, i.e., striated muscles, fat, and liver cells, they are stimulated by this hormone to take up more glucose and metabolize it. A rise in blood glucose levels concentration stimulates the beta cells to synthesize and release insulin hormones.
Notably, insulin has a wide range of effects that can be categorized as either growth-promoting or anabolic. Functions of insulin can also be categorized as turn on or turn off; some of the turn-on functions are;
Glucose storage in the liver
Synthesis of DNA
Use of glucose by the insulin-sensitive cells
Protein synthesis and uptake of amino acids
Some of the turn functions include
Glycogen breakdown in the liver cells
Breaks down fat
Role of incretins
These hormones are glucagon-peptide lookalike cells manufactured in the small intestines. Food intake is what triggers the secretion of these hormones. Before glucose levels rise, the incretins hormone kick in. the hormone also reduces the rate of nutrient absorption into the bloodstream through gastric emptying reduction.
Also, incretins hormone can increase satiety which leads to reduced food intake. Note, people ailing from type 2 diabetes have hormone incretins in lower supply. That is a possible explanation as to why most diabetic people claim to be constantly hungry. There are two types of incretin hormones;
GIP, i.e., Gastric Inhibitory Peptide
GLP-1, i.e., Glucagon-like peptide
A naturally occurring peptide called DDP4 (dipeptidyl peptidase-4) breaks down every peptide. An injectable diabetes drug, Exenatide, is identifiable as a glucagon-like peptide (GLP-1) that imitates the effects of glucose-lowering of the secretin when carbohydrate is orally ingested into the body.
Upon administering Exenatide, it significantly helps in reducing BG levels by imitating incretins. Also, both the short and the long-acting GLP-1 agents are being widely utilized. Some of the functions of incretins are;
Suppressing secretion of glucagon
Stimulating secretion of insulin
Increasing meal satiety to signal your brain when to stop eating
Prevent elevation of BG levels by slowing gastric emptying
DPP-4 enzymes are responsible for the quick deactivation of incretins on endothelial cell surfaces and in the bloodstream. That way, Incretins’ glucose-lowering effects last for some minutes.
DPP4 inhibitor is a new class of medication that blocks the enzyme from being broken down by incretins, thus prolonging incretins’ positive glucose suppression effects. Alternatively, another additional medication class is the dipeptidyl peptidase-4 is available for many orally administrable forms of products.
Damage of cells in the DM
Insulin resistance alongside a decrease in insulin secretion results in hyperglycemia responsible for most of the health complications associated with diabetes. Glucose overload causes acute health problems such as;
Hyperosmolar hyperglycemic state
Note that the above health problems are metabolic disorders. Feeding the body tissues too much glucose can lead to progressive but slow cellular damage, wound problems such as tissues injury, and chronic health problems associated with kidneys, eyes, nerves, and heart. Also, glucose toxicity results in hyperglycemic damage of the tissues. Some of the three common ways in which excess glucose can cause damage to the tissues are;
Unnecessary growth of blood cells is encouraged by protein kinase C, whose secretion is activated by excess intracellular glucose. That leads to the constriction of the blood vessels and thickening at the basement of these blood vessels membranes, which releases homocysteine and C-reactive protein molecules that are pro-inflammatory.
Oxidative stress and antioxidant intracellular activities’ effectiveness are reduced as a result of excess intracellular glucose. With that, there’s the neural oxidation damage, i.e., oxidation in the neurons.
Through glycosylation in excess glucose attaches to protein, e.g., glycosylated hemoglobin, which identifies the laboratory amounts of average glycemic levels, the inflammatory reactions of the glycosylated protein are triggered, injuring the blood vessels lining. Additionally, there is possible functional disruption at the thickening of the endothelial layers, membrane basement of the capillaries due to the sticking of the glycosylated proteins at the basement membrane of the capillaries.
Problems Associated with Insulin Resistance
Type 2 diabetes patients have a decrease in insulin response, commonly known as insulin resistance. The liver, adipose, and skeletal tissues take up and metabolize much lesser glucose than optimal for a similar amount of insulin. The liver doesn’t react to the usual insulin signals. That makes the liver secrete more than the usual glucose amount.
Before the manifestation of type 2 diabetes, insulin resistance can develop over many years without the patient’s realization. Note that propensity for insulin resistance is hereditary, with other health problems can intensify the condition significantly.
When skeletal muscles are exposed to excess free fatty acids, these cells will use up the fat for metabolism while using less and taking up more glucose than average despite an adequate supply of insulin.
With that, insulin effectiveness is decreased due to high blood lipid levels. That occurrence leads to overweight, high body fat, cholesterol, and obesity, which causes increased insulin resistance. Remember also that, physical-inactivity bears similar effects.
Note that obese and sedentary overweight people have muscles that have a high accumulation propensity for triglycerides. That, in turn, causes the body cells to prefer fat utilization to glucose in the production of muscular energy. Also, obesity and physical inactivity increase the resistance of insulin.
Beta Cell Dysfunction Problem
Because of the destruction of the beta cells, there’s no insulin production for people with type 1 diabetes. According to researchers, this is an off-center autoimmune response lynching an attack on the body’s immune system. Such a trigger has been linked to environmental triggers, milk, vaccines, bacteria, and viruses. Also, there’s a progressive decrease in insulin for people with type 2 diabetes.
That continuous availability decrease in insulin for type 2 diabetes patients results in direct progressive worsening of the ability of the beta cells to produce adequate amounts of insulin. The beta cells produce less insulin in type 2 diabetes patients’ conditions worsen; they also release that insulin slowly and in irregular patterns than healthy people.
Insufficient supply of insulin causes the tissues that absorb insulin, such as adipose tissues, skeletal muscle, and liver, not to efficiently clear glucose from the blood. So, the diabetic patient ends up suffering from severe hyperglycemia. The beta cells might secrete adequate insulin amounts to compensate for the insulin resistance-caused high demands.
However, with time, the defective batá cells will gradually decrease their insulin production to a point where they can’t cancel out the deficit. At this particular stage, the patient will be ailing from persistent hyperglycemia. For type 2 diabetic patients, their beta cells can no longer adapt to the prolonged peripheral insulin resistance demands.
With a downward trend preceding comes hyperinsulinemia and hyperglycemia that causes the beta cells to overstretch beyond their capability leading to their failure. As loss of functioning beta cells progressively increases in type 2 diabetes manifests itself as hyperglycemia.
Diabetes Effects on The Body Organs
As comprehensively highlighted above, diabetes is caused due to the body’s inability to use the available insulin or the body is not capable of manufacturing enough insulin. You already know that glucose is the primary source of the body due to what you eat.
So, the insulin hormone plays a significant role in glucose regulation. If you get an early diagnosis, you have a high chance of ensuring you have diabetes-related complications such as;
Nervous system complications
For people who have been ailing from diabetes for more than 25 years, neuropathy is a common problem associated with diabetes. Neuropathy can cause significant damage to the involuntary nervous control systems, such as digestion.
The most common form of this complication is peripheral neuropathy that causes pain and numbness in the;
Feet and toes
Arms and fingers
Complications With the Kidney and The Urinary System
With time, if blood sugar levels are not effectively regulated, it can cause improper filtering out of the waste from the bloodstream. Also, note that diabetic neuropathy is a kidney complication that affects many diabetic people.
Depending on your diabetic condition severity, research has shown a direct link between some skin conditions and diabetes. Some of these conditions can either be mild or server. For example, a person with elevated blood glucose levels may potentially have high levels of triglyceride in their blood.
A high concentration of that compound in the blood can lead to xanthomatosis with a red rash coupled with yellow lesions known as xanthomas. Some of the apparent signs and symptoms are;
Bacterial infections, e.g., boils
Control of blood sugar levels pogil like this one is ideal for evaluating when someone is experiencing high or low blood sugar levels. Typically, irregular secretion and ineffective control of blood sugar levels lead to diabetes. Some other signs and symptoms to indicate someone is diabetic include thirst for high blood sugar levels.