Pancreas Insulin hormone and glucose blood in cell
 |
| Pancreas Insulin hormone and glucose blood in cell |
In this article, we'll talk about the insulin hormone that is
secreted from the pancreas and its effect on the blood and glucose.
The pancreas is found deep inside the cavity, divided into a head,
body, and tail lying transversely behind the stomach, between the spleen and
duodenum. When the stomach is removed you'll see the long pancreas, with a head
tucked next to the primary turn of the duodenum or intestine and a tapered tail
next to the spleen. This location near the intestine allows it to simply
secrete the digestive enzymes for food processing.
The Endocrine Pancreas
Objectives:
▸ Identify the principal hormones
secreted from the endocrine pancreas, their cellsorigin
▸ Understand the nutrient, neural, and
hormonal mechanisms that regulate hormone
▸ List the principal target organs for
insulin and glucagon action and their effects.
▸ Identify the disease states caused
by oversecretion, undersecretion, or decreased sensitivity to insulin, and
describe the principal manifestations of every.
Embedded within the acini are richly vascularized, small clusters
of endocrine cells called the pancreatic islets or islets cells (islets of
Langerhans) which are located randomly throughout the pancreas. Carrots are
rich in blood vessels, this makes it easier to release hormones and facilitate
access to blood circulation. Additionally, they're innervated by
parasympathetic and sympathetic neurons, and nervous signals clearly modulate
secretion of its hormones . Pancreatic islets secretes the hormones insulin and
glucagon , with touch of hormone somatostatin , directly into the blood to
affect organs everywhere the body. All three of those hormones play a major
role in carbohydrate, fat, and protein metabolism. The target tissues for
pancreatic hormones:-
a. Insulin – liver, fatty tissue and
musculus cells;
b. Glucagon – Liver
Pancreatic Hormones :-
Insulin
A 51-amino-acid protein consisting of two aminoalkanoic acid chains
linked by disulfide bonds,
synthesized from proinsulin within the beta cells occupy the
central portion of the pancreatic islets of Langerhans and are surrounded by
alpha and delta cells . About one sixth of the secreted product remains within
the type of proinsulin which has no insulin activity. Once insulin secreted,
it's a half-life of about 6 minutes in order that it's mainly cleared in 10-15
minutes from circulation. Some binds receptors of target cells while the
remainder is degraded by liver and a few in kidneys. it's secreted into the
blood in response to arise in concentration of glucose or amino acids.
i. Insulin and carbohydrate metabolism:
a. Insulin is that the only major
hormone that induces glucose uptake. It stimulates the rapid transfer of glucose
within glut-4 tissues (sensitive insulin carrier) and stimulates the use of
glucose source of energy. Both effects cause decrease in plasma glucose
following insulin release.
b. Effects on the liver : insulin
increases hepatic glucose uptake to convert excess glucose into glycogen for
storage and it inhibits enzymes involved in glycogenolysis and gluconeogenesis.
Insulin also increases glucose oxidation( glycolysis : the metabolism of
glucose for generation of ATP (cellular energy)) .
ii. Insulin and metabolic process :
a. Effects on liver : insulin promotes carboxylic acid synthesis
from glucose within liver cells which are then transported to adipose cells for
storage, large amounts of fatty acids are utilized by the liver to make
triglycerides( the storage type of fat) and make their way through the blood to
be stored in fat cells, decreases ketogenesis and favors cholesterol
biosynthesis.
b. Effects on muscle : Insulin
inhibits the action of hormone-sensitive lipase which breaks down fats and
suppresses free carboxylic acid uptake (free fatty acids and glucose are
competitive substrates).
c. Effects on fatty tissue : Insulin
plays a significant role in energy storage in fatty tissue by stimulates fat
cells to make fats from fatty acids and glycerol, essentially within the type
of triglycerides, which represent 90% of the mass of fatty tissue. the general
net effect of insulin is an enhanced storage of fats (lipogenesis). Insulin
inhibits mobilization and oxidation of fatty acids and rapidly decreases circulating
triglycerides and inhibiting triglyceride breakdown. In fatty tissue, insulin
inhibits hormone sensitive triglyceride lipase activity. there's thus a marked
reduction in generation of ketoacids.
iii. Insulin and protein/amino acid metabolism :
a. Enhances amino uptake into liver
and muscle and reduces the breakdown of proteins . The general effect of
insulin on proteins is the cause of protein storage, not being used for energy
source.
b. Stimulates the incorporation of
all amino acids into proteins (protein synthesis) in muscle.
c. Increases the quantity and
translation efficiency of ribosomes ( messenger RNA), thus forming new proteins.
d. Increases the speed of
transcription of DNA within the nucleus to make increased quantities of RNA,
ultimately forming new proteins.
Regulation of insulin synthesis and secretion :
i. the most important stimulators of insulin synthesis and release are:-
1. Increases in plasma glucose.
2. Increases in high plasma energy
(proteins, ketostead, fatty acids, triglycerides).
3. Increases in gastrointestinal
peptides by food intake .
4. Parasympathetic or epinephrine
system acetylcholine stimulation.
c. Effects on muscle : the most
important sites of insulin action are cardiac and muscle, insulin stimulates
glucose transport by increasing both the activity and number of GLUT-4
transporters and insulin also reduces blood sugar levels by stimulating
glycolysis, additionally as insulin stimulates the synthesis of protein in
muscle.
d. Effects on fat : within the fat
cell, Insulin promotes glucose transport into the fat cells and stored as
glycogen or metabolism to triglyceride.
ii. Insulin-manufacturing inhibitors and secretions are:
1. Decreases in plasma glucose.
2. Decreases in plasma energy
substrates.
3. Somatostatin
4. Sympathetic system norepinephrine stimulation.
Glucagon:
A 29-amino-acid polypeptide hormone is
produced and secreted by the alpha cells of the pancreas. Glucagon is
stimulated by lack of glucose related to fasting states and by sympathetic
stimulation. Alternatively, glucagon is inhibited by insulin secretion, by
eating, or by the presence of hyperglycemia. Glucagon could be a hormone that
has the subsequent major effects:-
It should be noted that glucagon has the alternative effects of insulin.
i- it increases hepatic synthesis of
glucose from pyruvate, lactate, glycerol, and amino acids ,a process is named
gluconeogenesis, which raises the plasma glucose level.
ii- It stimulates the formation of
glucose from glycogen, fats, and proteins within the liver, a process is named
glyconeogenesis , gluconeogenolysis
(conversion of glycogen to glucose within the liver) so releasing of glucose to
the blood from liver cells, that also raises the plasma glucose level.
iii- it increases the breakdown of fat
triglyceride by increases lipolysis, increase activity and release of free
fatty acids, raising the plasma levels of fatty acids and glycerol.
iv.
Inhibits glycolysis.
The major stimulators of glucagon synthesis and release are:
i. Amino acids released after
ingestion of a protein meal(high protein, low carbohydrate meal)
are major secret glucagon at the α cell.
ii. Physiologic stimuli are decreases
plasma glucose and other plasma energy
substrates ie. ketoacids, fatty acids, triglycerides, decreases in insulin.
iii. Parasympathetic and sympathetic
system activity.
iv. Stress and exercise.
The major inhibitors of glucagon synthesis and release are :-
i. Increases in plasma glucose,
ii. Increases in plasma energy
substrates,
iii. Increases in insulin
Somatostatin or GHIH
It secreted by the pancreatic δ cells (delta cells) of the
pancreas, it suppresses human growth hormone secretion, also suppresses insulin, glucagons, gastrin,
vasoactive intestinal peptide or VIP.
Regulation of blood sugar Levels
Insulin acts to lower blood sugar levels by allowing the glucose to
flow into cells. Glucagon acts to lift blood sugar levels by causing glucose to
be released into the circulation from its storage sites. Insulin and glucagon
act in an opposite but balanced fashion to stay blood sugar levels stable.
Hyperglycemic effects of glucagon and therefore the hypoglycemic effects of
insulin.
Why is blood sugar regulation so important?
It is the most important nutrient that is used by the brain, retina
and epithelium tumors of the gonads in good quantities to get their energy. Any
small amounts made by liver between meals is employed for metabolism of the
brain only, otherwise, it might attend muscles and other tissues and leave the
brain with no nutrition.
Hypoglycemic
lethargy,
vision problems-acute, tired, dizzy
Hyperglycemia
(chronic)
regeneratius recital with cellular dehydration, loss of sugars in urine and
fluids, loss of body electrolytes and fluids, dehydration in the body. DM (DM)
Insulin deficiency results in the event of DM.
There are two kinds of DM
Type 1 (insulin-dependent
diabetes mellitus = IDDM ) and its onset is typically in childhood (juvenile
onset or diabetes ). Type 2 (non–insulin-dependent DM = NIDDM ) , and
its onset is typically later in life (maturity onset).
The three cardinal signs of DM are :
Polyuria –huge urine output
Polydipsia –excessive thirst
Polyphagia –excessive hunger and food consumption
As well as loss of weight
and Asthenia(lack of energy) .
Type 1 diabetes is that the
results of an auto‐immune disease where the person's own system attacks the beta cells
within the Islets of Langerhans. This reduces the quantity of insulin that the
pancreas can release and a whole lack of insulin, it's treated by insulin
injections. When blood sugar levels rise after a meal, the glucose cannot enter
cells to be used for energy. These patients must inject insulin after every
meal to facilitate glucose uptake into cells. If not, blood sugar levels are
very high while the cells need glucose because they can't enter the cell
without insulin .... ---10% of diabetes
cases.
Type 2 diabetes is thanks to the desensitization of insulin
receptors thanks to chronically high blood sugar levels and over insulin
production, 90% of diabetes cases. For sick people develop insulin resistance
and fail target cells to respond to insulin thanks to down-regulation receptors
. major risk factors are heredity, age (40+). Treated with programs for weight
loss through diet and exercise, exercise is even simpler at insulin receptor
resensitization than any drug. Some patients are helped by oral medications
(like glucophage) that decrease intestinal absorption of glucose, decrease
hepatic glucose production and improve target cell sensitivity to insulin.
Pathological physiology of Diabetes mellitus:
1) Loss of glucose within the urine, glycosuria, dehydrating effect of Elevated blood sugar in diabetics
. Two of the
first manifestations of diabetes are excessive urination and excessive thirst.
They demonstrate how the out-of-control levels of glucose within the blood
affect kidney function. The kidneys are to blame for filtering glucose from the
blood. Excessive blood sugar draws water into the urine. Use body water to
relieve urine leaves the body dried, then the person is unusually thirsty and
continuously. The person can also continue
hunger because the body cells are unable to access the glucose within
the bloodstream. Over time, constantly high proportions of intra-blood glucose
injure tissues throughout the body, in blood vessels and nerves.. Inflammation
and injury of the liner of arteries result in atherosclerosis and an increased
risk of coronary failure and stroke. Damage to the microscopic blood vessels of
the kidney impairs kidney function and might result in nephropathy. Damage to
blood vessels that serve the eyes can result in blindness. vas damage also
reduces circulation to the limbs, whereas nerve damage ends up in a loss of
sensation, called neuropathy, particularly within the hands and feet. Let's
know that changes increase the chance of infection, infection, and dying tissue
(necrosis), this causes a high rate of dismount and foot declines in the leg in
patients with diabetes.
2) Acidosis in diabetics.
Uncontrolled diabetes can result in a dangerous style of acidosis
called ketoacidosis. The shift from CHO to metastasis increases in diabetics,
the amount of acetone body, β- oxybutyric acid and ketones (are a metabolic
breakdown product of carboxylic acid metabolism, some cells will use fatty
acids for fuel if glucose isn't available which are converted by the liver to
ketones) increases which ends up in
increase acid content of the blood that may be utilized in cell respiration,
but cells aren't ready to utilize them rapidly so ketones accumulate within the
blood. Ketones are acids, and lower the pH of the blood as they
accumulate. During a state of glucose
deficiency, the liver is forced to use another pathway using fat that causes
increased production of ketones inside the blood to be ketoacidosis., When
these acids in diabetes are not controlled by concentration, the condition may
lead to an acid coma and death within hours.
Hyperinsulin
Increased insulin injections or increased secretion due to
pancreatic osmosoblastoma, associated signs and symptoms are:
i. Hypoglycemia as a results of
hyperinsulinemia .
ii. Sympathetic activation (secretion
of epinephrine) by the hypoglycemia causing rapid pulse rate, nervousness,
sweating, hunger.
iii. Increase in body weight (you'll
know insulin is an anabolic hormone).
iv. Central system dysfunction.
Glucagon excess
is that the
results of production and release of the alpha cell tumors. Associated signs
and symptoms are:-
i. Weight loss, distinctive roseola,
elevated plasma glucose and ketoacidosis.
ii. Reduced plasma aminoalkanoic acid.
iii. Increased urinary nitrogen.
ليست هناك تعليقات:
إرسال تعليق