Pancreas Insulin hormone and glucose blood in cell

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.