Small slogan of pancreas

Pancreas pancreas: a large, slender, grape-shaped gland located behind the stomach and between the spleen and duodenum; Its right end (pancreatic head) is large and downward, its left end (pancreatic tail) is horizontal, and its tail faces the spleen. Exocrine or pancreatic juice of pancreas is imported into duodenum through pancreatic duct, and pancreatic juice contains various digestive enzymes. There are also scattered island cell groups in the pancreas, called islets or Langerhans islands. Pancreatic islet β cells secrete insulin, which promotes hypoglycemia and hepatic glycogen synthesis. Glucagon secreted by islet α cells can promote the decomposition of hepatic glycogen and raise blood sugar. Insulin and glucagon feed back each other to control blood sugar in a small range. If insulin is absolutely or relatively insufficient for any reason, it will lead to diabetes.

Langerhans is the endocrine part of the pancreas, and it is a large number of cell clusters with different sizes and shapes, which are scattered all over the pancreas. Hormones produced by islets become insulin, which can control carbohydrate metabolism. If insulin secretion is insufficient, you will suffer from diabetes.

Islets can secrete hormones such as insulin and glucagon. References:

Islet human islet cells are mainly divided into A cells, B cells, D cells and PP cells according to their staining and morphological characteristics. A cells account for about 20% of islet cells and secrete glucagon. B cells account for 60%-70% of islet cells and secrete insulin; D cells account for 10% of islet cells and secrete somatostatin; PP cells are few in number and secrete pancreatic polypeptide.

1. Insulin Insulin is a small molecule protein with 5/kloc-0 amino acids and its molecular weight is 6000. Insulin molecules have a chain (265,438+0 amino acids) and a chain (30 amino acids) which are bound by two disulfide bonds. If the disulfide bond is opened, it will lose its activity. B cells first synthesize a large molecule of proinsulin, then process it into 86-peptide proinsulin, and then hydrolyze it into insulin and connecting peptide (C peptide). Insulin and C-peptide are released into the blood, and a small amount of proinsulin enters the blood, but its biological activity is only 3%-5% of insulin, while C-peptide has no insulin activity. Because C-peptide is produced in the process of insulin synthesis, its quantity has a parallel relationship with insulin secretion, so measuring the content of C-peptide in blood can reflect the secretory function of B cells. The serum insulin concentration of normal people in fasting state is 35- 1.45 pmol/L, and the half-life of insulin in blood is only 5 minutes, which is mainly inactivated in the liver, and muscles and kidneys can also inactivate insulin. 1965, China biochemists synthesized insulin with high biological activity for the first time, which became the first pioneering work to synthesize living organisms (protein) in human history.

(I) Biological Effects of Insulin Insulin is the main hormone to promote anabolism and regulate blood sugar stability.

1. Regulation of glucose metabolism: Insulin promotes the uptake and utilization of glucose by tissues and cells, accelerates the synthesis of glycogen from glucose, stores it in liver and muscle, inhibits gluconeogenesis, promotes the conversion of glucose into fatty acids, and stores it in adipose tissue, resulting in the decrease of blood sugar level. When insulin is deficient, the blood sugar concentration will increase, and if it exceeds the renal sugar threshold, sugar will appear in urine, causing diabetes.

2. Regulation of fat metabolism Insulin promotes the synthesis of fatty acids in the liver and then transports them to fat cells for storage. Under the action of insulin, fat cells can also synthesize a small amount of fatty acids. Insulin also promotes glucose to enter fat cells, which can not only synthesize fatty acids, but also convert them into α -glycerophosphate. Fatty acids and α -glycerophosphate form triglycerides, which are stored in fat cells. At the same time, insulin also inhibits the activity of lipase and reduces the decomposition of fat. When insulin is deficient, there will be disorder of fat metabolism, enhanced lipolysis, increased blood lipid, accelerated fatty acid oxidation in the liver, and a large number of ketone bodies will be generated. Because of the disorder in the process of sugar oxidation, ketone bodies can not be well treated, leading to ketosis and acidosis.

3. Regulation of protein metabolism Insulin promotes the synthesis of protein, which can be used in all aspects of protein synthesis:

① Promoting the transmembrane transport of amino acids into cells;

② It can accelerate the process of nuclear replication and transcription, and increase the production of DNA and RNA;

③ Acting on ribosomes, accelerating the translation process and promoting the synthesis of protein; In addition, insulin can inhibit protein decomposition and liver gluconeogenesis. Because insulin can enhance the synthesis process of protein, it can also promote the growth of the body. However, when insulin acts alone, it does not promote growth very strongly, and only with auxin can it play an obvious role. Recent research shows that almost all cells in the human body have insulin receptors on their cell membranes. Insulin receptor has been successfully purified and its chemical structure has been clarified. Insulin receptor is a tetramer composed of two α subunits and two β subunits. The α subunit is composed of 7 19 amino acids, which is completely exposed outside the cell membrane and is the main site of receptor binding to insulin. α and α subunits, α and β subunits are bonded by disulfide bonds. The β subunit consists of 620 amino acid residues and is divided into three domains: N-terminal 194 amino acid residues extend out of the membrane; In the middle is a transmembrane domain containing 23 amino acid residues; The C-terminal extends to the inside of the membrane, which is the protein kinase domain. Insulin receptor itself has tyrosine protein kinase activity, and insulin binding to the receptor can activate the enzyme, phosphorylating tyrosine residues in the receptor, which plays a very important role in transmembrane information transmission and cell function regulation. A series of reactions caused by insulin binding to receptors are quite complex and unclear.

(b) Regulation of insulin secretion

1. The role of blood sugar Blood sugar concentration is the most important factor in regulating insulin secretion. When the blood sugar concentration increases, insulin secretion increases obviously, thus promoting blood sugar reduction. When the blood sugar concentration drops to the normal level, insulin secretion quickly returns to the basic level. Under the stimulation of persistent hyperglycemia, insulin secretion for 5 minutes can be divided into three stages: within 5 minutes after hyperglycemia, insulin secretion can be increased by about 10 times, mainly due to the release of hormones stored in B cells, so the duration is not long, and insulin secretion will be reduced by 50% after 5- 10 minutes; After the blood sugar rises 1.5 min, the insulin secretion increases for the second time, reaching the peak in 2-3 hours, lasting for a long time, and the secretion rate is much higher than that in the first period, which mainly activates the insulin synthase system of B cells and promotes synthesis and release. If hyperglycemia lasts for about a week, insulin secretion can be further increased, which is caused by long-term hyperglycemia stimulating B cell proliferation.

2. The role of amino acids and fatty acids Many amino acids have the effect of stimulating insulin secretion, among which arginine and lysine have the strongest effect. When the blood sugar concentration is normal, the content of amino acids in the blood increases, which can only slightly stimulate the secretion of insulin, but if the blood sugar increases, excessive amino acids can double the insulin secretion caused by blood sugar. When Una's fatty acids and ketone bodies increase greatly, it can also promote insulin secretion.

3. Hormones that affect insulin secretion mainly include:

① Gastrointestinal hormones, such as gastrin, secretin, cholecystokinin and gastrin, can promote insulin secretion, but the first three can only promote insulin secretion at pharmacological dose, unlike a physiological stimulus. Only GIP or glucose-dependent insulin stimulating polypeptide can regulate insulin secretion. GIP is a linear polypeptide composed of 43 amino acids secreted by duodenal and jejunal mucosa. Experiments show that GIP can stimulate insulin secretion in a glucose-dependent manner. The hyperglycemia caused by oral glucose and GIP secretion are parallel, and this parallel relationship leads to rapid and obvious insulin secretion, which exceeds the insulin secretion reaction caused by intravenous glucose. Some people inhaled glucose into the mouth of rats and injected GIP antiserum, which led to an increase in blood sugar concentration, but the insulin level did not increase significantly. Therefore, GIP can be considered as the main incretin stimulating factor secreted by the intestinal mucosa during the absorption of glucose by the small intestine. Besides glucose, intestinal absorption of amino acids, fatty acids and hydrochloric acid can also stimulate the release of GIP. Some people call the relationship between gastrointestinal hormones and insulin secretion "intestinal-islet axis", which has important physiological significance, so that insulin secretion has increased while food is still in the intestine, preparing for the utilization of sugar, amino acids and fatty acids to be absorbed from the small intestine;

② Auxin, cortisol, thyroid hormone and glucagon can indirectly stimulate insulin secretion by increasing blood glucose concentration, so long-term high-dose application of these hormones may lead to B cell failure and diabetes;

③ The growth inhibition of islet D cells can at least inhibit the secretion of insulin and glucagon through paracrine, and glucagon can also directly stimulate B cells to secrete insulin. Fig. 1 1-22 Distribution of islet cells and interaction between hormones → Prompt promotion →→→ Prompt inhibition of GIH: somatostatin 4. Neuroregulatory islets are innervated by vagus nerve and sympathetic nerve. Stimulation of vagus nerve can directly promote insulin secretion through acetylcholine acting on M receptor. Vagus nerve can also indirectly promote insulin secretion by stimulating the release of gastrointestinal hormones. When sympathetic nerve is excited, norepinephrine acts on α2 receptor to inhibit insulin secretion. Second, glucagon Human glucagon is a linear polypeptide consisting of 29 amino acids, with a molecular weight of 3485, which is also derived from the cleavage of a macromolecular precursor. The concentration of glucagon in serum is 50- 100ng/L, and its half-life in plasma is 5- 10min. Glucagon is mainly inactivated in liver and degraded in kidney.

(1) Glucagon has the opposite effect to insulin, and it is a hormone that promotes catabolism. Glucagon has a strong role in promoting glycogen decomposition and gluconeogenesis, thus significantly increasing blood sugar. 1mol/L hormone can rapidly decompose 3× 106mol/L glucose in glycogen. Glucagon activates hepatocyte phosphorylase through cAMP-PK system and accelerates glycogen decomposition. The enhancement of gluconeogenesis is because hormones accelerate the entry of amino acids into hepatocytes and activate the enzyme system related to gluconeogenesis. Glucagon can also activate lipase, promote lipolysis, strengthen fatty acid oxidation and increase ketone body production. The target organ of glucagon that produces the above metabolic effects is the liver. These effects will disappear when the liver is removed or the blood flow to the liver is blocked. In addition, glucagon can also promote the secretion of insulin and islet somatostatin. Pharmacological dose of glucagon can increase cAMP content in myocardial cells and enhance myocardial contraction.

(II) Regulation of Glucagon Secretion There are many factors that affect glucagon secretion, and blood glucose concentration is an important factor. When blood sugar decreases, pancreatic secretion of glucagon increases; When blood sugar rises, glucagon secretion decreases. The effect of amino acids is opposite to that of glucose, which can promote the secretion of glucagon. Protein powder or intravenous injection of various amino acids can increase glucagon secretion. On the one hand, the increase of amino acids in blood can promote the release of insulin, thus reducing blood sugar, on the other hand, it can also stimulate the secretion of glucagon, which has certain physiological significance for preventing hypoglycemia. Insulin can indirectly stimulate the secretion of glucagon by lowering blood sugar, but the islet secreted by B cells can directly act on neighboring A cells than somatostatin secreted by D cells, and inhibit the secretion of glucagon. Insulin and glucagon are a pair of hormones with opposite effects, and they both form a negative feedback regulation loop with blood sugar level. Therefore, when the body is in different functional states, the molar ratio (I/G) of insulin to glucagon in blood is different. Generally, the I/G ratio is 2.3 under overnight fasting, but it can be reduced to below 0.5 under hunger or long-term exercise. The decrease of the ratio is caused by the decrease of insulin secretion and the increase of glucagon secretion, which is beneficial to glycogen decomposition and gluconeogenesis, maintaining blood sugar level, adapting to the needs of the heart and brain for glucose, being beneficial to fat decomposition and enhancing the energy supply of fatty acid oxidation. On the contrary, after eating or sugar loading, the ratio can rise above 10, which is due to the increase of insulin secretion and the decrease of glucagon secretion. In this case, the effect of islet ratio is the main one.

Pancreas 1 small pancreatic organ "shoulders the heavy responsibility.

There is a very small organ deep in our upper abdomen, that is, the pancreas. Although the pancreas is small, it plays an extraordinary role. It can be said to be one of the most important organs of the human body. The reason why the pancreas is one of the most important organs in human body is that it is a gland with both internal and external secretion functions, and its physiological function and pathological changes are closely related to life.

The pancreas "lives in seclusion" behind the peritoneum, and its popularity is far less than that of its neighboring stomach, duodenum, liver and gallbladder. However, several digestive enzymes secreted by pancreas play a leading role in food digestion, especially in fat digestion.

In terms of secretion, although the pancreas is small, it contains endocrine cells with multiple functions, such as secreting glucagon, insulin, gastrin and motilin. The hormones secreted by these cells not only participate in the digestion and absorption of substances, but also regulate the physiological functions of the whole body. If these cells are pathological and secrete too much or too little substance, symptoms will appear.

Diet, guidance and disease prevention are the basis.

Wang Zaitong, director of general surgery department of Beijing Hospital, told reporters that the incidence of pancreatitis in China is lower than that in foreign countries, which is because of different eating habits.

The main causes of pancreatitis are alcoholism, trauma and biliary tract diseases. Alcoholism is the main cause of pancreatitis abroad, but in China it is mainly due to the poor drainage and reflux of pancreatic juice caused by gallstones, which makes the pancreas inflamed. In recent years, the incidence of pancreatitis in China has increased. Among them, pancreatitis caused by gallstones, that is, biliary pancreatitis, accounts for more than 50% of patients.

The causes of bile formation are also very complicated, and there are differences at home and abroad. For example, the formation mechanism of cholesterol stones and bile pigment stones is very different. Now with the improvement of living standards of residents, gallstones caused by improper diet have also increased. Therefore, the methods to prevent gallstones are very clear. One is to improve the hygiene level, and the other is to eat less foods with fat and high cholesterol.

In addition to gallstones, overeating is also an important pathogenic factor of acute pancreatitis. Overeating promotes pancreatic juice secretion, and alcohol directly stimulates pancreatic juice secretion. When alcohol enters the duodenum, it will cause papilla edema and Oddi's sphincter spasm, so there is no way for pancreatic juice to "digest" the pancreas itself. Patients with cholelithiasis can also have acute pancreatitis due to bile reflux or poor pancreatic juice. Clinically, most patients with acute pancreatitis have the experience of overeating. Therefore, whenever meat and vegetables are mixed, the diet is reasonable.

To sum up, in order to prevent pancreatitis, the most important thing is to reduce drinking, prevent or treat biliary diseases in time, avoid overeating to reduce the burden on pancreas, avoid trauma and so on.

3 Hold down the vicious killer! -Be alert to acute and chronic pancreatitis.

Director Wang Zaitong said that acute pancreatitis can be divided into edema type and hemorrhagic necrosis type. Edema is characterized by sudden and persistent pain in the upper abdomen after overeating, which is gradually relieved after 3 ~ 5 days of treatment. Hemorrhagic necrosis is serious, and even a few patients go into shock when the symptoms of upper abdominal pain are not manifested, and suddenly die of respiratory failure, with a mortality rate of more than 40%! Chronic pancreatitis has three obvious characteristics, one is emaciation, the other is fatty diarrhea, and the third is pain, manifested as epigastric pain. The pain is mild and heavy, and it is persistent. The pain is more severe after eating. In addition, because the pancreas belongs to the retroperitoneal organ, it also has pain, that is, low back pain. Suffering from pancreatitis, there are generally surgical and non-surgical treatments. Surgical treatment includes ampulloplasty, Oddi sphincter plasty, biliary and intestinal drainage, gallstone removal and total pancreatectomy. Non-surgical treatment, that is, drug treatment, includes: analgesia; Correct malnutrition; Abstinence from alcohol; Adjust diet, limit fat intake, supply exocrine enzymes and endocrine of pancreas. Although the cure rate of acute severe pancreatitis has been improved, the treatment cost is very high, which requires hundreds of thousands of yuan and takes a long time to recover. It belongs to the most serious necrosis in acute abdomen.

Keep your mouth shut, be vigilant and strengthen nutrition. You can't just cut it off.

Even if patients with acute pancreatitis have returned to normal diet after treatment, it does not mean that their bodies have fully recovered. Therefore, postoperative recovery, conditioning and follow-up are very important. Eliminate the reasons in time. In China, most acute pancreatitis is caused by biliary tract diseases. Therefore, after the condition of acute pancreatitis is stable and the patient's general condition gradually improves, biliary calculi should be actively treated. Alcoholic pancreatitis patients, the first thing is to ban alcohol, if you drink again, it is undoubtedly a chronic suicide. Those who overeat and lead to pancreatitis should avoid repeating the same mistakes. Patients with pancreatitis caused by hyperlipidemia should take lipid-lowering drugs for a long time and have a low-fat and light diet. Regular follow-up to prevent complications. In the recovery period of pancreatitis, inflammation only subsides, and inflammatory exudates often take 3 ~ 6 months to be completely absorbed. During this period, some patients may have complications such as pancreatic cyst and pancreatic fistula. If the patient finds that the abdominal mass is enlarged, and there are symptoms such as abdominal pain, bloating, hematemesis and vomiting. He needs to see a doctor in time. Strengthen nutrition and promote recovery. If the exocrine function of the pancreas is not obviously damaged, you can eat some foods mainly containing carbohydrates and protein to reduce the intake of fat, especially animal fat. If the exocrine function of the pancreas is impaired, nutrition can be properly strengthened with the help of pancreatin preparation.

There are many dietary taboos.

For patients with acute pancreatitis, special attention should be paid to diet. In the acute phase, you should completely fast, and when the symptoms are gradually relieved, you can eat lipoprotein-free liquids, such as juice, lotus root starch, rice soup, vegetable juice, noodle soup and so on. And then you can gradually switch to low-fat semi-liquid liquid. In addition, patients must avoid greasy foods, such as fat, peanuts, walnuts, sesame seeds, cakes, etc., avoid irritating and spicy foods, and absolutely ban alcohol. The treatments for acute pancreatitis include radish juice, water chestnut juice, honeysuckle juice and fresh potato juice. Such as fresh potato juice: wash and chop, mash, wrap with gauze and juice, and take 1 ~ 2 spoonfuls on an empty stomach.

Pancreatitis leads, followed by diabetes.

Protein is one of the important nutrients necessary for human body, especially animal protein, and it is a high-quality protein. However, if a large amount of protein is ingested in one meal, it may cause severe acute pancreatitis. If you eat a lot of protein food and drink too much wine at the same time, you will have a greater chance of causing acute pancreatitis. Dr. Sun Meizhen from the Department of Endocrinology, Beijing Hospital said that if you eat a lot of protein and fatty foods at one time in a short time, it will stimulate the pancreas to secrete a lot of pancreatic juice quickly, and the pancreatic duct will not be able to discharge so much pancreatic juice into the duodenum for a while. In addition, if the original pancreatic duct is not smooth, pancreatic juice will flood and flow into pancreatic tissue. If you add the stimulation of wine, it will aggravate the situation of pancreatic juice flooding. This will lead to the digestion of the pancreas itself, leading to death. In mild cases, part of the pancreas will also be irreversibly damaged. After suffering from acute pancreatitis, the internal and external secretion function of pancreas is often damaged to varying degrees. Exocrine dysfunction is characterized by decreased digestive function, especially the ability to digest fat and protein. Patients with loss of appetite, weight loss, abdominal distension, diarrhea, and often accompanied by characteristic steatorrhea. This damage to exocrine function is usually not easy to recover, so pancreatin replacement therapy can only be used in treatment. And impaired pancreatic endocrine may lead to diabetes. The possibility of diabetes depends on the degree of inflammation of pancreatitis. If it is edematous pancreatitis, it will recover quickly, while if it is acute necrotizing pancreatitis, it will affect the function of pancreatic insulin secretion, making insulin secretion too little or even no, which will lead to diabetes. This kind of diabetes caused by other diseases is called secondary diabetes. Therefore, it is also very important to protect the pancreas if you want to avoid diabetes.