Insulin Glargine, which is marketed under the name Lantus, among others, is a long-acting insulin, used in the management of type I and type II diabetes. All the details about Insulin Glargine is described below.
Type I Diabetes-dependent insulin mellitus (IDDM) / juvenile-onset diabetes mellitus: There is damage to B cells in the islet of the pancreas: most cases are autoimmune (type 1A) antibodies that destroy B cells can be detected in the blood, but there are also idiopathic (type 1B ) -Not cell B antibodies are found. In all cases type 1 circulating insulin levels are low or very low, and patients are more susceptible to ketosis. This type is less common and has a low genetic predisposition.
Type II Noninsulin-dependent diabetes mellitus
(NIDDM)/maturity onset diabetes mellitus:
I There is no loss or only moderate reduction
in B cell mass; low insulin circulation.
Normal or even high, no B-cell antibodies can be proven; have a high level of genetic predisposition; generally have a late onset (past middle age). More than 90% of cases of diabetes type 2 diabetes. The cause may be: Abnormalities in B cell gluco receptors so that they respond with higher glucose concentrations or relative B cell deficiency. Either way, insulin secretion is disrupted; may progress to B cell failure.
Reduced sensitivity (relative resistance);
of peripheral tissues to insulin: reduction
in number of insulin receptors, i.s. 'down
regulation of insulin receptors. Many hyper
tensions are hyperinsulinaemic, but normally
anemic; and have associated dyslipidaemia,
hyperuricemia, abdominal obesity (metabolic
syndrome). Thus, there is relative insulin
resistance, particularly at the level of liver,
muscle and fat. Hyperinsulinemia per se
has been implicated in causing angiopathy.
ACTIONS OF INSULIN
The overall effects of insulin are to dispose meal derived glucose, amino acids, fatty acids and favour storage of fuel. It is a major anabolic hormone: promotes synthesis of glycogen, Lipids and protein. The actions of insulin and the results of its deficiency can be summarized as:
1. Insulin facilitates glucose transport across
cell membrane: skeletal muscle and fat are
highly sensitive. The availability of glucose L
intracellularly is the limiting factor for its
utilization. However, glucose entry in liver,
brain, RBC, WBC and renal medullary cells is
Largely independent of insulin. Ketoacidosis
Interferes with glucose utilization by brain and
contribute to diabetic coma. Muscular activity
induces glucose entry in muscle cells without need for insulin. As such, exercise has
insulin sparing effect.
The intracellular pool of vesicles contain
ing glucose transporter glycoproteins GLUT4
(insulin activated) and GLUT1 is in dynamic
equilibrium with the GLUT vesicles inserted into the membrane. This equilibrium is regulated by insulin to favour translocation to the membrane.
Moreover, on a long-term basis, synthesis of
GLUT4 is upregulated by insulin.
2. The first step in intracellular utilization of
glucose is its phosphorylation to form glucose
6-phosphate. This is enhanced by insulin through increased glucokinase production. Insulin facilitates the synthesis of glycogen from glucose in the liver, muscles and fat by stimulating the enzyme glycogen synthase. It also inhibits glycogen degrading enzyme phosphorylase decreased glycogenolysis in liver.
Hopefully this information would help you!
Conclusion
As old insuline preparation which are not more used now.
Just because their peak effect and also similar to physiological appearance of insulin.
It has to be during meal which are provided by these new insuline analogues like insuline glargine or insulin aspart.
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