What Is Inhaled Insulin?

The endocrine portion of the pancreas is an irregular population of cells scattered throughout the pancreas. There are at least three types of cells in the islets: A (or a2) cells secrete glucagon; B (or ) cells secrete insulin; another type of cell has recently been found, called D (or or 1) cells, which under normal conditions Growth hormone release inhibiting hormone. When D cells proliferate or develop tumors, they secrete a large amount of gastrin, which is called gastrinoma. Can cause peptic ulcer with excessive gastric acid secretion. These cells of the islets abut tightly on the capillaries, and the secreted hormones penetrate the blood through the capillaries to regulate the glucose metabolism.

The endocrine portion of the pancreas is an irregular population of cells scattered throughout the pancreas. There are at least three types of cells in the islets: A (or a2) cells secrete glucagon; B (or ) cells secrete insulin; another type of cell has recently been found, called D (or or 1) cells, which under normal conditions Growth hormone release inhibiting hormone. When D cells proliferate or develop tumors, they secrete a large amount of gastrin, which is called gastrinoma. Can cause peptic ulcer with excessive gastric acid secretion. These cells of the islets abut tightly on the capillaries, and the secreted hormones penetrate the blood through the capillaries to regulate the glucose metabolism.

Chinese name

Islets

Foreign name

pancreatic islets

Secreted hormone

Insulin, glucagon

Composition form

Many cell clusters of varying sizes and shapes

Owning system

Endocrine System

Function

Regulation of blood sugar stabilization

Islet I. Physiological anatomy of islets:

1. Pancreatic islets are endocrine cell clusters distributed among the acinars of the pancreas exocrine area, which are distributed throughout the pancreas and are unevenly distributed, with the pancreatic tail being the largest. The islets vary in size, with only a few cells in the small and hundreds of cells in the large. There are also scattered endocrine cells located near the acinus and ducts. There are about 500,000 islets in humans, accounting for 1-2% of the pancreatic volume. Islets are homologous to the exocrine pancreas, and dorsal and ventral pancreatic buds protrude from the foregut caudal endoderm. Most of the epithelial cells in the two pancreatic buds form the exocrine part; a part of the cells are dispersed in the exocrine part, and islets are formed. In recent years, it has been proposed that islets originate from neural crest cells that have migrated into the pancreatic primordium early in the embryo, but it is still controversial.

2. The islets are coated with a thin layer of reticular fibers, but the coating is not complete. The cells of the islets are arranged into cords, and the capillaries between the cords are abundant. Cells are smaller than acinar cells, appear polygonal and round, vary in size, and have light cytoplasmic staining. Nuclear circle, located in the center of the cell, with dense chromatin particles. With special staining methods, B cells, A cells and D cells can be distinguished in humans and some animals. Electron microscopy and immunohistochemical studies also found PP cells and D1 cells. In addition to C cells, several other cells are known to secrete peptide hormones. A series of scholars have included them in the APUD cell system and they have been included in the gastrointestinal and pancreatic endocrine system. Their organelles are underdeveloped and are mainly characterized by secretory particles. The morphology and structure of various cells' secreted particles have their own characteristics.

3. There are abundant porous capillaries in the islets. In recent years, it has been found that the arteries that enter the pancreas first divide into capillaries in the islets, then merge into veins and divide into capillaries between the acinars of the exocrine part, forming the islet-acinar portal system. The blood flow from the islets to the acinus contains high concentrations of insulin and glucagon, which regulates the exocrine activity of the pancreas. The islets have cholinergic and adrenergic nerve endings, the former may promote B cell secretion and the latter may promote A cell secretion.

4. The secretion of islet cells is regulated by blood glucose levels, gastrointestinal hormones and nerves. When the blood glucose level is high, it stimulates B cells to secrete insulin, and when the blood glucose level is low, it stimulates A cells to secrete glucagon. Incretins, glucagons, and gastric inhibitory peptides promote B-cell secretion. Growth hormone release inhibiting hormone inhibits B and A cell secretion. In normal times, the vagus nerve promotes B and A cells to secrete a small amount of hormones to keep blood glucose at a normal level; when the sympathetic nerve is excited, it inhibits B cells, promotes A cells, and increases blood glucose levels.

Islet II, the main role of insulin

Insulin mainly acts on the liver, muscle and adipose tissue, and controls the metabolism and storage of three major nutrients: protein, sugar and fat.

(1) Effect on glucose metabolism. It can accelerate the use of glucose and inhibit the production of glucose, even if the blood glucose goes out and the source decreases, so the blood glucose decreases.

Speed up glucose utilization. Insulin can increase the permeability of the cell membrane to glucose, promote the transport of glucose from the outside into the cell, provide favorable conditions for the use of sugar in the tissue, and promote the activities of glucokinase (intrahepatic) and hexokinase (extrahepatic), and promote glucose It is transformed into glucose 6 phosphate, which accelerates the hydrolysis and oxidation of glucose; and promotes the synthesis and storage of liver glycogen and muscle glycogen under the action of glycogen synthase.

Inhibit the production of glucose, inhibit the decomposition of liver glycogen into glucose, and inhibit the conversion of glycerol, lactic acid and amino acids into glycogen, and reduce the gluconeogenesis.

(2) Effect on fat metabolism. Promote fat synthesis and storage, inhibit fat breakdown. In diabetes, glucose metabolism is impaired, a large amount of fat is mobilized, and a large amount of free fatty acids are oxidized to acetyl-CoA in the liver, and then become ketone bodies. If too many ketone bodies are produced, ketemia occurs. Insulin can inhibit lipolysis and promote the use of sugar, thereby inhibiting ketone body production and correcting ketemia.

(3) Effect on protein metabolism. Promote protein synthesis and prevent protein breakdown.

(4) Insulin can promote potassium and magnesium ions to pass through the cell membrane into the cell; it can promote the synthesis of DNA, RNA and ATP.

In addition, glucose in and out of red blood cells and brain cell membranes, glucose reabsorption in renal tubules, and small intestinal mucosal epithelial cells' glucose absorption are not affected by insulin. The target cells for insulin include liver cells, fat cells, muscle cells, blood cells, lung and kidney cells, and testicular cells.

Islet III, insulin-related indications

1. Insulin analogues Type 1 diabetic patients, due to impaired islet -cell function and insulin secretion are absolutely inadequate. Insulin treatment is required at the time of onset, and life-long insulin replacement therapy is required to maintain life. About 5% of the total number of people with diabetes. On the basis of lifestyle and oral hypoglycemic drug combination therapy, patients with type 2 diabetes can start combination therapy with oral drugs and insulin if their blood sugar has not reached the control target. In general, when HbA1c is still greater than 7.0% after a combination of large doses of multiple oral drugs, insulin therapy can be considered. Wasting patients with new onset and difficult to distinguish from type 1 diabetes. In the course of diabetes (including newly diagnosed type 2 diabetes), when there is no obvious cause of weight loss, insulin therapy should be used as soon as possible. For patients with first-onset type 2 diabetes with high blood sugar, it is difficult to achieve satisfactory blood glucose control with oral drugs, and rapid relief of hyperglycemic toxicity can partially reduce insulin resistance and reverse -cell function, so newly diagnosed type 2 diabetes is associated with Intensive insulin therapy can be used when there is significant hyperglycemia. There are also some special cases where insulin treatment is also required: perioperative period; when severe acute complications or stress states occur, temporary use of insulin is needed to pass the dangerous period, such as diabetic ketoacidosis, hypertonic hyperglycemia, Lactic acidosis, infection, etc .; severe chronic complications such as diabetic foot, severe diabetic nephropathy, etc .; combined with some serious diseases, such as coronary heart disease, cerebrovascular disease, blood disease, liver disease, etc .; women with gestational diabetes and diabetes with pregnancy During pregnancy, before and after childbirth, and during lactation, if the blood sugar cannot be controlled by diet alone, the insulin therapy should be used and oral hypoglycemic drugs should be disabled. People with secondary and specific diabetes.

2. Adverse reactions caused by excessive injection

If you inject too much insulin during treatment, it will lead to hypoglycemia. When the poisoning is mild, it mainly affects the autonomic nervous system, manifested as hunger, dizziness, paleness, weakness, and sweating, but also tremor, discomfort in the heart area, face and limbs Numbness and headache. When the blood sugar is further reduced, it affects the central nervous system, dysphonia, diplopia, muscle tremor, ataxia, and subsequent coma and convulsions of varying degrees. This state is called insulin shock, which can be fatal if not rescued in time. .

Islet IV. Insulin injection site

The abdomen is the part that should be selected first because the subcutaneous fat in the abdomen is thicker, which can reduce the risk of injection into the muscle layer. It is the easiest to pick up the abdominal skin, and it is also the fastest place to absorb insulin. It should be injected 3 to 4 fingers away from the sides of the belly button. The thinner the subcutaneous layer is, the easier it is to penetrate into the muscle layer. This area is most suitable for injection of short-acting insulin or mixed and mixed insulin.

In addition, the outer thigh, the upper quarter of the upper arm, and the buttocks are also suitable sites for insulin injection.

Outer thigh: Thigh injection can only be performed from the front or the outer side, and there are more blood vessels and nerves distributed on the inner side. It is not suitable for injection. When injecting the thigh, be sure to pinch the skin or use a super-fine, ultra-short (5 mm) pen needle.

The outer quarter of the upper arm: This is the most unsuitable site for self-injection, because the subcutaneous tissue of the upper arm is thin and easy to inject into the muscle layer: you cannot pick up the skin by yourself during self-injection. When the upper arm must be injected, it is recommended to use an ultra-fine and ultra-short pen needle (5 mm) or to assist the injection by medical staff and family members.

Buttocks: Buttocks are suitable for injecting medium- and long-acting insulin (such as medium-acting insulin injected before bedtime), because the subcutaneous layer of the buttocks is thick and the absorption of insulin is slow. There is no risk of intramuscular injection from the skin.