Insulin binds to the insulin receptor subunit a on the target cell membrane

② Phosphorylation of tyrosine residues in the β subunit of the insulin receptor activates tyrosine protein kinase in the receptor

③Activated tyrosine protein kinase phosphorylates the tyrosine residues of the intracellularly coupled insulin receptor substrate (IRS) protein

④ Step-by-step signal transduction through IRS downstream signaling pathways such as phosphoinositide 3-kinase (P13-K) and mitogen-activated protein kinase (MAPK) triggers protein kinase and phosphatase cascade reactions, ultimately causing biological effects and some gene transcription and expression

Insulin resistance is a decrease in the sensitivity of insulin target cells to insulin, that is, a larger amount of insulin is required to achieve normal physiological effects.

Clinical insulin resistance is one of the important causes of the development of diabetes, hypertension, hyperlipidemia and other diseases.

Insulin is a key hormone that promotes substance anabolism and maintains stable blood sugar concentration.

It is of great significance to the storage of energy substances and growth and development of the body.

The target tissues of insulin are mainly liver, muscle and adipose tissue

normal blood sugar concentration

Promote glycogen decomposition and inhibit glycogen synthesis

Inhibit gluconeogenesis

Promote the transport and oxidative utilization of glucose in peripheral tissues

Insulin promotes fat synthesis and storage

Insulin inhibits lipolysis and utilization

Insulin inhibits protein breakdown

Insulin promotes protein synthesis

Regulation of blood glucose

Regulatory effects of amino acids and fatty acids in blood

islet hormone

gastrointestinal hormones

other hormones

Pancreatic islet cells are dually innervated by vagus nerve and sympathetic nerve

Neuromodulation has little effect on normal insulin secretion

Glucagon is a hormone that promotes the catabolism of substances and mobilizes the breakdown of energy substances in the body to provide energy.

The main target organ of glucagon is the liver

① Promote hepatic glycogenolysis, reduce hepatic glycogen synthesis and enhance gluconeogenesis, and increase blood sugar levels.

② Reduce the synthesis of triglycerides from fatty acids in the liver, promote the decomposition of fatty acids, and increase the production of ketone bodies.

Inhibits protein synthesis in the liver and promotes its decomposition. At the same time, it increases the amount of amino acids entering liver cells and accelerates amino acid synthesis. Conversion of acid to glucose increases gluconeogenesis

Effects of blood sugar

Effect of amino acids

Insulin and somatostatin can directly inhibit glucagon secretion from adjacent α cells

Hormone regulation: Insulin can also indirectly stimulate glucagon secretion by lowering blood sugar.

Among gastrointestinal hormones, cholecystokinin and gastrin can promote glucagon secretion, while secretin has the opposite effect.

When sympathetic nerves are excited, glucagon secretion is promoted through beta receptors on the pancreatic islet a cell membrane.

When the vagus nerve is excited, it inhibits glucagon secretion through M receptors

Early stage nonspecific insulitis Pancreatic islet lesions: late B cell granule loss, vacuolar degeneration, necrosis, and disappearance

Early lesions are not obvious, late B cells are reduced Cap, small arteries, basement membrane thickening, blood vessel wall thickening, hyaline degeneration Fibrinoid necrosis and increased vascular permeability

Due to insufficient insulin and inappropriate elevation of glycemic hormone, symptoms of polyuria, polydipsia, polydipsia, and fatigue may worsen in the days before onset. In the decompensation stage, loss of appetite, nausea, vomiting, and abdominal pain occur, often accompanied by symptoms such as headache, irritability, and drowsiness. Breathing is deep and rapid, and the exhaled breath smells like rotten apples (acetone smell). As the disease progresses, severe water loss occurs, decreased urine output, dry skin and mucous membranes, sunken eyeballs, fast and weak pulse, decreased blood pressure, and cold limbs; in the advanced stage, various reflexes become slow or even disappear, and eventually coma.