Pathogenesis of insulin resistance as seen in a patient with type II DM

Pathogenesisof insulin resistance as seen in a patient with type II DM

Inmost of the cases, problems associated with insulin resistance andsecretion leads to the pathophysiological conditions. Before type 2diabetes develops, the rate at which insulin is secreted goes down.Decrease in glucose response is the initial phases of insulinsecretion and low amounts of insulin secreted after meals causesimpaired glucose tolerance (IGT) (Nolan et al., 2011). Most of thedoctors will order oral glucose tolerance test of which the resultsare used to determine the level of insulin resistance in anindividual. Patients in the United States usually indicate an overresponse to this condition. Studies on patients in different parts ofthe world have shown that persons with obesity show a decrease insecretory responses.

Impairedinsulin secretion usually takes place step by step and involveslipotoxicity and glucose toxicity. Patients with such clinicalmanifestations may suffer from decreased pancreatic beta cell mass.With time, control of blood glucose becomes very hard. Raisedpostprandial may sometimes be seen in patients in early stages oftype 2 diabetes due to rising insulin resistance among other factors(Nolan et al., 2011). Patients with insulin resistance conditions areunable to exert actions related to the concentration of insulin inthe blood. As such the major organs of the body such as the liver areaffected.

Inhuman beings, insulin works mainly through the insulin receptors andgrowth factors such as growth factor-1 (IGF-1) receptor. Tyrosinekinase b of insulin is normally activated when insulin binds to asubunit. The activities initiated by kinase are vital inautophosphorylating and controlling the actions controlled by insulin(Scheen, 2014). The following factors are responsible for controllinghow the insulin receptor work ambient insulin levels diseases andvarious physiological states. When insulin resistance is high, thelevel of insulin secreted in the blood also goes up to ensure thelevel of glucose is maintained. Insulin also helps in controllinglipid homeostasis (Scheen, 2014). The response to insulin resistanceis mediated by some factors that send signals to the pancreatic Bcells these signals are responsible for appropriate insulin levels.The signals inability to respond to insulin sensitivity results inuncontrolled levels of insulin in the blood.

Signalmediators that controls insulin response have been identified theyinclude hormones of the gut, fat-derived hormones, free fatty acids,and glucose. The mechanism such as elevated insulin degradation,autoantibodies to insulin and primary cell target defects amongothers are the causes of insulin resistance syndromes (Scheen, 2014). Mitochondria in the body cells plays a vital role in generatingenergy. Therefore, any defect in mitochondrial cells may alsocontribute to problems in insulin resistance.

Inmost of the developing countries, obesity has been identified as oneof the leading causes of insulin resistance. In obese people, thereis a high possibility of having a reduced number of receptors. Thepost receptors may also not be in a position to activate the tyrosinekinase (Steven &amp Taylor, 2012). Two hormones responsible forenergy balance in the body include leptin and ghrelin. Leptinsuppresses food intake thus inducing weight loss. On the other hand,ghrelin plays a role in meal initiation. Obese people are resistantto leptin, but they have a low level of circulating ghrelin hormone(McKenney &amp Short, 2011).

Conclusion

Insulinfunction is to allow the body to use glucose from the food we eatespecially the carbohydrates to generate energy. Insulin is releasedfrom the pancreas when the levels of sugar are high in the bloodafter taking meals. People with problems in insulin secretion cannotregulate the amount sugar in their bodies and, therefore, ends uphaving type 2 diabetes.

References

McKenney,R. L., &amp Short, D. K. (2011). Tipping the balance: thepathophysiology of obesity and type 2 diabetes mellitus. SurgicalClinics of North America,91(6),1139-1148.

Nolan,C. J., Damm, P., &amp Prentki, M. (2011). Type 2 diabetes acrossgenerations: from pathophysiology to prevention and management. TheLancet,378(9786),169-181.

Radder,J. K., Lemkes, H. H. P. J., &amp Krans, H. M. J. (2012).Pathogenesisand Treatment of Diabetes Mellitus.Dordrecht: Springer Netherlands.

Scheen,A. J. (2014). Pathophysiology of type 2 diabetes. ActaClinica Belgica.

Steven,S., &amp Taylor, R. (2012). Pathophysiology of type 2 diabetes. Type2 Diabetes.

Pathogenesis of insulin resistance as seen in a patient with type II DM

Pathogenesisof insulin resistance as seen in a patient with type II DM

Inmost of the cases, problems associated with insulin resistance andsecretion leads to the pathophysiological conditions. Before type 2diabetes develops, the rate at which insulin is secreted goes down.Decrease in glucose response is the initial phases of insulinsecretion and low amounts of insulin secreted after meals causesimpaired glucose tolerance (IGT) (Nolan et al., 2011). Most of thedoctors will order oral glucose tolerance test of which the resultsare used to determine the level of insulin resistance in anindividual. Patients in the United States usually indicate an overresponse to this condition. Studies on patients in different parts ofthe world have shown that persons with obesity show a decrease insecretory responses.

Impairedinsulin secretion usually takes place step by step and involveslipotoxicity and glucose toxicity. Patients with such clinicalmanifestations may suffer from decreased pancreatic beta cell mass.With time, control of blood glucose becomes very hard. Raisedpostprandial may sometimes be seen in patients in early stages oftype 2 diabetes due to rising insulin resistance among other factors(Nolan et al., 2011). Patients with insulin resistance conditions areunable to exert actions related to the concentration of insulin inthe blood. As such the major organs of the body such as the liver areaffected.

Inhuman beings, insulin works mainly through the insulin receptors andgrowth factors such as growth factor-1 (IGF-1) receptor. Tyrosinekinase b of insulin is normally activated when insulin binds to asubunit. The activities initiated by kinase are vital inautophosphorylating and controlling the actions controlled by insulin(Scheen, 2014). The following factors are responsible for controllinghow the insulin receptor work ambient insulin levels diseases andvarious physiological states. When insulin resistance is high, thelevel of insulin secreted in the blood also goes up to ensure thelevel of glucose is maintained. Insulin also helps in controllinglipid homeostasis (Scheen, 2014). The response to insulin resistanceis mediated by some factors that send signals to the pancreatic Bcells these signals are responsible for appropriate insulin levels.The signals inability to respond to insulin sensitivity results inuncontrolled levels of insulin in the blood.

Signalmediators that controls insulin response have been identified theyinclude hormones of the gut, fat-derived hormones, free fatty acids,and glucose. The mechanism such as elevated insulin degradation,autoantibodies to insulin and primary cell target defects amongothers are the causes of insulin resistance syndromes (Scheen, 2014). Mitochondria in the body cells plays a vital role in generatingenergy. Therefore, any defect in mitochondrial cells may alsocontribute to problems in insulin resistance.

Inmost of the developing countries, obesity has been identified as oneof the leading causes of insulin resistance. In obese people, thereis a high possibility of having a reduced number of receptors. Thepost receptors may also not be in a position to activate the tyrosinekinase (Steven &amp Taylor, 2012). Two hormones responsible forenergy balance in the body include leptin and ghrelin. Leptinsuppresses food intake thus inducing weight loss. On the other hand,ghrelin plays a role in meal initiation. Obese people are resistantto leptin, but they have a low level of circulating ghrelin hormone(McKenney &amp Short, 2011).

Conclusion

Insulinfunction is to allow the body to use glucose from the food we eatespecially the carbohydrates to generate energy. Insulin is releasedfrom the pancreas when the levels of sugar are high in the bloodafter taking meals. People with problems in insulin secretion cannotregulate the amount sugar in their bodies and, therefore, ends uphaving type 2 diabetes.

References

McKenney,R. L., &amp Short, D. K. (2011). Tipping the balance: thepathophysiology of obesity and type 2 diabetes mellitus. SurgicalClinics of North America,91(6),1139-1148.

Nolan,C. J., Damm, P., &amp Prentki, M. (2011). Type 2 diabetes acrossgenerations: from pathophysiology to prevention and management. TheLancet,378(9786),169-181.

Radder,J. K., Lemkes, H. H. P. J., &amp Krans, H. M. J. (2012).Pathogenesisand Treatment of Diabetes Mellitus.Dordrecht: Springer Netherlands.

Scheen,A. J. (2014). Pathophysiology of type 2 diabetes. ActaClinica Belgica.

Steven,S., &amp Taylor, R. (2012). Pathophysiology of type 2 diabetes. Type2 Diabetes.