The quality of life is determined by the Health and Diseases. There are various ailments /conditions that put life in trouble which could range from systemic disorders to cancer. In the present context, metabolic disorder type 2 diabetes mellitus was discussed. Diabetes is a metabolic disorder that results when sufficient insulin is not produced by the pancreas (WHO Report, 2009).
This condition also results if insulin is not utilized by the body (WHO Report, 2009). Insulin is type of hormone that has control on blood sugar (WHO Report, 2009). The level of blood sugar raises and leads to Hyperglycaemia, when the diabetes is not manageable and finally causes destruction to blood vessels and nerves (WHO Report, 2009).
There are two types of Diabetes most common in the population. They are type 1 and type 2.Type 2 diabetes also known as non-insulin-dependent or adult-onset occurs when body fails to use insulin. Nearly 90% of diabetic individuals are present globally which is the merely the reflection of the result of physical inactivity and over body weight (WHO Report, 2009). Although, the symptoms of Type 2 diabetes are same as that of Type 1, it may take many years to get diagnosed after the onset (WHO Report, 2009).
Type 2 diabetes most frequent in adults but in the modern society children are also falling victims to this disorder. The present day life style is exposing wide range of individuals to develop various disorders where type 2 Diabetes is the frequent. The causes of this disorder are not completely understood although clinical data persists. This could be due to the existence of multiple factors that could predispose the people to diabetes.
The inclusion criteria for type 2 diabetic individuals could be elevated glucose levels observed in fasting or post lunch sessions. The exclusion criteria would for those with normal values. The parameters that help in understanding the development of type 2 diabetes may be those that reflect levels of blood glucose, insulin, lipid, other suspected agents with genetic etiology etc. There is need to carry out a thorough literature review.
Therefore, keeping in view of the above background information, the topic was selected and there is need to carry out a thorough literature review. Recently, it was reported that Insulin resistance (hyperinsulinemia) is the sole factor and could play important role in the development of type 2 diabetes mellitus (Jannetta et al., 2010).
This was revealed when patients with type 2 diabetes had pulsatile arterial compression when retromastoid craniectomy of Brain was performed (Jannetta et al., 2010). These patients gradually have shown improvement of glucose regulation (Jannetta et al., 2010).
Thus, when right anterolateral medulla region gets compressed it could lead to type 2 diabetes mellitus (Jannetta et al., 2010). In children with Type 2 diabetes, it was reported that a sort of insulin resistance marked by pubertal rise and insufficient beta-cell insulin response could lead to hyperglycemic condition (Banerji, 2002). Adult individuals have a low response to glucose levels intravenously and delay in oral glucose oral response Loss of beta cell function is reported in adults but not in children (Banerji, 2002).
To investigate this problem, the researchers have supplemented mixed meal and given glucagon intravenously and performed oral glucose tolerance test (Banerji, 2002).This resulted in the significant restoration of alpha and beta cell function with good C- peptide response indicating that they are essential in the diagnosis of type 2 diabetes mellitus(Banerji, 2002).
The pathophysiology of Type 2 diabetes has genetic basis. In an experiment New Zealand obese (NZO) mouse was chosen as a model of type 2 diabetes. By employing lean strains, researchers have detected many quantitative trait loci (QTL) susceptible for hyperglycemia (Joost, 2010).The transcription factor Zfp69, the genes RabGAP, Tbc1d1 were Lepr, Pctp, Abcg1, and Nmur2 identified(Joost, 2010).They were considered as the candidate genes in sequencing investigations (Joost, 2010).
Since, Type 2 diabetic individuals are presented with fasting and postprandial hyperglycemia much research emphasis was given in this context (Rizza, 2010). Glucose synthesis is high prior to eating and does not to get diminish after a diet in type 2 diabetes(Rizza, 2010). This could be due to the fact that altered impaired insulin produced suppression of endogenous glucose synthesis.
High rates of glycogenolysis and gluconeogenesis play role to develop hepatic insulin resistance (Rizza, 2010). These stages of carbohydrate metabolism get altered leading to decreased hepatic glucose uptake and hepatic glycogen production which are insulin stimulated processes (Rizza, 2010). This also leads to low uptake of extracellular glucose due to poor activation of hepatic glucokinase.
Finally, there would be delayed or very slow insulin secretion that could lead to increased glucose concentrations at the peak level(Rizza, 2010). This occurs due to altered suppression of glucagon. Thus, insulin resistance increases the time period of hyperglycemia (Rizza, 2010). The therapy of type 2 diabetes has become a complex task. Although, there is knowledge about the occurrence of the disease and risk factors, thorough metabolic control type 2 diabetes is lacking (Triplitt , 2010).
This needs an assessment of clinical inertia which is considered as a failure to begin or further the therapy (Triplitt, 2010). This strategy is for those patients who are unable to receive the care in an evidence-based approach. Hence, this aspect serves as a important factor in the therapeutic management of type 2 diabetes (Triplitt, 2010).
Further, there are several reasons for the clinical inertia and they are inter associated among the diabetic individuals, care providers, and health systems and from definite treatment approaches (Triplitt, 2010). Very often, antihyperglycemic agents also contribute to the clinical criteria (Triplitt, 2010).
This takes place due to the self reactive drugs and their side effects like gastrointestinal discomfort, edema, weight gain, hypoglycemia and finally the complexity treatment regimen (Triplitt, 2010). There is no independent therapy to cease the pancreatic beta-cell defect, as such treatments in a combined manner could be necessary involving thiazolidinediones and glucagon-like protein-1 agonists that are connected to prolonged A1C level decrease.
This aspect has good implications for the diagnosis of type 2 diabetes mellitus (Triplitt , 2010). Recently, it was described that incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are potential in the management of type 2 diabetes mellitus(Knop , Vilsbøll, & Holst 2009).
This is because , the actions of GLP-1 and GIP, have tremendous therapeutic effect on the enhancement of meal driven insulin secretion and trophic effects on the beta-cell GLP-1 reduces glucagon secretion, and diminishes food intake and appetite (Knop , Vilsbøll, & Holst 2009). Thus, two novel drug classes are related to potential benefits of incretin hormones and are recommended for treating T2DM (Knop , Vilsbøll, & Holst 2009).
Here, long-acting stable analogues of GLP-1 which are injectibles incretin mimetics, and oral inhibitors of dipeptidyl peptidase 4 (DPP4; the enzyme responsible for the rapid degradation of GLP-1 and GIP), belong to the category of incretin enhancers (Knop , Vilsbøll, & Holst 2009). This was strengthened by another report that emphasized the physiological role of incretin hormones (William, 2010).
The two classes of incretin-directed therapies are exert their action by enhancing increasing endogenous levels of glucagon-like peptide-1 (GLP-1) or by resembling the action of endogenous GLP-1 (ie, GLP-1 agonists) (William, 2010). Since the management of type 2 diabetes mellitus (T2DM) is a complex process, incretin therapy could be a key therapy as it does not induce bogy weight increase and hypoglycemia as seen in conventional therapies (William, 2010).
Therefore, it is reasonable to mention that incretin related parameters could serve as novel diagnostic markers and help reduce the burden of type 2 diabetes mellitus. Adult individuals are becoming more favorable targets and contributing the rising prevalence and incidence of type 2 diabetes mellitus (DM) (Chen et al., 2010).This could be due to age associated complications like weakness multiple comorbidities, and functional defects(Chen et al., 2010).
Insluin resistance plays role in predicting weakness and diabetes increases loss of muscular power (Chen et al., 2010).Thus, for aged people with type 2 DM , there is a need to consider multiple factors like physical discomfort, tube feeding, cognitive defects. Here, glycemic control of these patient could raise the chances of hypoglycemia and significant functional decrease (Chen et al., 2010).
Thus, diagnosing type 2 diabetes mellitus in old individuals is a complex process and need further research on new emerging parameters that reflect hypo or hyperglycemia and insulin resistance.
In conclusion, Type 2 diabetes is a metabolic disorder with emerging etiological factors that vary in response to changing life style or environmental hazard exposure. The pathophysiology of this disorder is interrelated with carbohydrate metabolism. As such, parameters that indicate the normal o abnormal levels of glucose, insulin, should be considered from all corners of the investigation. The cause of diabetes may also have genetic susceptibility.
Large number of individuals from children to the old age is now becoming targets of this disorder. There is a need to undertake appropriate screening programs to precisely identify the type 2 diabetic individuals. Concomitant factors like obesity, cardiovascular problems mat also further aggravate the problem, contributing to the overall incidence. An evidence based approach is more suggestive for proper diagnosis.
Type 2 Dabetes. WHO report. Web.
Banerji, M,A. 2002. Impaired beta-cell and alpha-cell function in African-American children with type 2 diabetes mellitus – “Flatbush diabetes”.J Pediatr Endocrinol Metab. 15 Suppl 1:493-501.
Chen, L,K., Chen, Y, M., Lin, M, H., Peng, L, N., Hwang, S, J. 2010. Care of elderly patients with diabetes mellitus: A focus on frailty. Ageing Res Rev. 2010
Jannetta, P, J., Fletcher, L, H., Grondziowski, P,M., Casey, K,F., Sekula, R,F Jr. 2010. Type 2 diabetes mellitus: A central nervous system etiology. Surg Neurol Int, 16;1. pii: 31.
Joost, H,G 2010. The genetic basis of obesity and type 2 diabetes: lessons from the new zealand obese mouse, a polygenic model of the metabolic syndrome. Results Probl Cell Differ. 52:1-11.
Knop, F, K., Vilsbøll, T., Holst, J, J. 2009. Incretin-based therapy of type 2 diabetes mellitus. Curr Protein Pept Sci. 10(1):46-55.
Rizza, A. 2010. Pathogenesis of Fasting and Postprandial Hyperglycemia in Type 2 Diabetes: Implications for Therapy. Diabetes.
Triplitt, C. 2010. Improving treatment success rates for type 2 diabetes: recommendations for a changing environment. Am J Manag Care 16(7 Suppl):S195-200.
William T. Cefalu M, D. 2010. The Physiologic Role of Incretin Hormones: Clinical Applications.2010. JAOA • 110 (3).8-14.