Diabetes, Type 2. Treatment Approaches Evaluation


Type 2 diabetes mellitus has become a serious health concern in recent period.

Since it has a strong connection with the other disorders its aetiopathogenesis is reported to involve a wide range of risk contributing factors.

There is a need to identify various treatment options for preventing the diverse clinical problems reported to contribute to the incidence of this metabolic disorder.

Biomedical database Pubmed was searched to retrieve pertinent literature on various treatment strategies.

It was found that type 2 diabetes has a plethora of promising treatment options.

Drug therapy in combination and adjunctive approaches has gained much attention with special emphasis on oral antidiabetics.

Mostly weight-reducing therapy was given prior importance due to the association of type 2 diabetes with obesity. Modification of diet with appropriate nutritional supplements was suggested. Other reliable treatment approaches are the utility of immune markers, genes, and hormone therapy.


Type 2 diabetes mellitus is a chronic and debilitating disease that was characterized by insulin resistance, impaired insulin secretion, and hyperglycemia and afflicting at least 171 million people worldwide. Patients with diabetes suffer from numerous microvascular and macrovascular complications which cause a lot of morbidity and mortality (Mudaliar, 2007). Its main clinical abnormalities include hepatic glucose production, peripheral insulin resistance, and defective beta-cell secretory function (Mudaliar & Edelman, 2000).

Its increase in prevalence is due to its association with several other metabolic abnormalities such as central obesity, hypertension, and dyslipidemia (Edelman, 1998). It has a wide range of etiological factors believed to initiate from the biochemical, genetical, and immunological abnormalities. As this disorder is mainly concerned with the defects in glucose and insulin regulation, significant therapeutic focus on these aspects has become mandatory for many years. But with the progressing complexity of this disorder, providing an effective remedy has become a challenging task to many diabetologists and scientists.

Although significant advancement has been made in treating the patients, there is some scarcity concerned with the available treatment options due to unawareness or fears of side effects. There is a need to address the existing concerns of this particular class of metabolic illness, which may require the input of different streams of life sciences as their contribution is proven to be reliable in modulating and refining the treatment. Since the clinical symptoms of type 2 diabetes are believed to manifest in association with other disorders, a wide range of treatment strategies would be a possibility. Therefore, the present description is mainly focused on reviewing the literature to explore and evaluate the various treatment approaches of type 2 diabetes mellitus.

Review of literature

Diabetes Mellitus is an important common health disorder. It comprises type 1 and type2 categories. This review focuses on the different treatment methods of Type 2 diabetes mellitus which is believed to have a strong link with other complications.

Initially, therapeutic interventions have started concentrating on diet and exercise. It was reported that the foundation therapy for this class of diabetes consists of regular exercise along with a diet consisting of 40% to 50% complex carbohydrates, 10% to 20% protein, and monounsaturated fats such as canola oil and olive oil (Edelman, 1998).

Steyn et al. (2004) further supported the role of diet and lifestyle in the prevention of type 2 diabetes. They reported that physical inactivity, overweight, and obesity; abdominal obesity is associated with the increased risk. Therefore, it was suggested that the normal weight status in the lower body mass index range of 21-23 and regular physical activity be maintained throughout adulthood so that abdominal obesity could be prevented with a saturated fat intake of less than 7% of the total energy intake.

Since it was reported that obesity and aging are associated with the increased risk of type 2 diabetes, research findings have revealed that weight loss therapy improves beta-cell function, lowers plasma glucagon concentrations, and improves insulin action in obese older adults. These metabolic effects are likely to reduce the risk of developing type 2 diabetes in this population (Villareal et al., 2008). Therefore, it may indicate that there is a need of implementing regular weight loss therapy for diabetic patients with appropriate diet and exercise.

Mudaliar and Edelman (2000) reported that insulin resistance plays a major role in patients with type 2 diabetes and described the importance of oral therapeutic approaches such as oral insulin secretagogues and insulin sensitizers in maintaining glycemia for varying periods when they are used independently and in combination.

This report has indicated that insulin therapy is very much reliable because of the progressive nature of the disease and the progressive decline in pancreatic beta-cell function. However, this article also added that insulin therapy may not be suitable in all cases especially in elderly individuals and those with co-morbid conditions, thus suggesting appropriate modifications in the goal of the therapy. Further, drug therapy has some promising applications and may need attention.

Reasner (1999) highlighted the association between obesity and type 2 diabetes mellitus and mentioned the importance of weight-reducing agents such as serotonin- and noradrenaline-reuptake inhibitor sibutramine, noradrenergic anorexiants, orlistat, leptin, and beta3-agonists.

It may indicate that the drugs aimed at treating obesity may indirectly exert potential benefits in treating type 2 diabetes. The other drugs considered are Repaglinide which is a new, fast-acting insulin secretagogue and pramlintide (an amylin analog), and glucagon-like peptide thiazolidinediones (troglitazone, rosiglitazone, and pioglitazone) which improve insulin resistance in patients whose diabetes is poorly controlled by diet and exercise therapy (Reasner, 1999). Plosker and Figgitt (2004) especially focused on Repaglinide known with other names such as Prandin, NovoNorm, and GlucoNorm. They reported that it is the first meglitinide analog to become available for use in patients with type 2 diabetes mellitus.

Therefore the use of Repaglinide as monotherapy or in combination with other antidiabetic agents, such as metformin or rosiglitazone, was reported to achieve good metabolic control, similar to that achieved with comparable glibenclamide (anti-diabetic drug) regimens. But this drug may require confirmation for assessing potential long-term advantages versus other agents, such as reducing cardiovascular complications. Similarly, the study by Reasner has cautioned the use of certain drugs due to the risk of side effects.

Troglitazone was used to decrease plasma glucose levels when given independently but is more effective in combination with sulphonylureas, metformin, or insulin. But, this drug has been associated with severe idiosyncratic hepatocellular injury (Reasner, 1999). Therefore, there is a need to consider the safety of many other therapeutic formulations designed for treating type 2 diabetes.

Next, it was reported that oral antidiabetic drugs are effective for controlling this type of diabetes because of their heterogeneous mode of action, safety profiles, and tolerability (Krentz & Bailey, 1999). These agents are sulphonylureas and rapid-acting secretagogues that stimulate insulin secretion, biguanides for reducing hepatic glucose production, alpha-glucosidase inhibitors that delay digestion and absorption of intestinal carbohydrates, and thiazolidinediones that improve insulin action.

It was further reported that oral antidiabetic therapy would ensure maintain long-term glycaemic control for overweight or obese patients in combination with insulin therapy (Krentz & Bailey, 1999). A recent report has described that a major proportion of type 2 diabetic patients require insulin to maintain glycemic control although there is widespread usage of oral antidiabetic agents (Levy, 2007).

It was indicated that to facilitate the transition to insulin therapy there may be a need for education to develop knowledge about the available insulin analogs (rapid-acting, long-acting, and premixed) with more predictable time-action profiles than human insulin preparations and simple-to-use insulin delivery devices.

It was also inferred that the selection process about insulin therapy could also help patients achieve recommended glycemic goals while minimizing hypoglycemia (Levy, 2007).

Therefore, it is reasonable to infer that there is a need for the patients with type 2 diabetes to develop awareness about the therapeutic regimen and transitions that might enable them to avoid any long-term delay associated with the wrong drug selection.

The use of insulin therapy has become a question previously as it was described that it failed to safely restore near-normoglycemia in the majority of patients (Edelman & Weyer, 2002).

In addition, it was also described that Amylin, a second beta-cell hormone that is secreted with insulin in response to meals is deficient in patients with insulin-requiring type 2 diabetes.

To overcome this defect researchers have identified pramlintide, a soluble, nonaggregating synthetic peptide analog of human amylin. Pramlintide was found to reduce postprandial glucose excursions and HbA (1c) levels in patients with type 2 diabetes thus improving the long-term glycemic control with a significant reduction in body weight (Edelman & Weyer, 2002). Therefore, pramlintide may act as a substitute for amylin and as adjunctive therapy to insulin by fulfilling some of the unaddressed clinical needs of insulin-using patients with type 2 diabetes. (Edelman & Weyer, 2002). Hence, the use of Pramlintide could be promoted without any hindrances.

Further, it was reported that a condition known as secondary failure is reported to deteriorate glucose control in patients on oral antidiabetic drugs mainly due to the progressive decline in beta-cell function and reduction in insulin secretion. (Stonehouse, Holcombe & Kendall DM, 2006). For this purpose, a novel drug named incretin mimetics (e.g. exenatide and liraglutide) was identified which targets insulin secretion, and thiazolidinediones which act on insulin resistance. It was found that only incretin-mimetics have a lowering HbA1c action, due to the improvement in beta-cell function which is coupled to significant weight loss (Stonehouse, Holcombe & Kendall DM, 2006).

Penfornis, Borot, and Raccah (2008) described that oral therapy with glucagon-like peptide-1 (GLP-1) inhibitors or analogs such as sitagliptin and vildagliptin is beneficial for the management of type 2 diabetes as they were found to lower HbA levels.

This therapy was especially reported to be effective as an alternative for patients who fail to tolerate other drugs like metformin and for those with inadequate control with maximal tolerated oral multi-therapies. This was further strengthened by another report that underscored the use of glucoregulatory properties of the intestinal incretin hormone glucagon-like peptide-1 (GLP-1).

Exenatide, a new drug of therapeutic class incretin mimetics, was reported to improve glycemic control by acting on the vital organs involved in glucose homeostasis.

It stimulates insulin secretion and suppresses glucagon secretion in a glucose-dependent way, slows gastric emptying, and reduces food intake (Guerci & Martin, 2008).

It ultimately produces significant reductions in fasting and postprandial hyperglycemia leading to a reduction of HbA1c levels accompanied by weight loss.

Since the diet is found to be vial for type 2 diabetic patients, there is a need to consider nutrition therapy with significant emphasis on calories that might improve the condition of the patient.

Jiang (2008) reported that calorie restriction prolongs life span and produces required metabolic profile for treating diseases such as type 2 diabetes. As such sirtuin 1(SIRT1), an NAD (+)-dependent deacetylase, was identified as a principal modulator of calorie restriction that produces beneficial effects on glucose homeostasis and insulin sensitivity (Jiang, 2008). Its main function was reported to enhance the activity of multiple proteins.

It was found that Resveratrol, a polyphenolic SIRT1 activator has potential implications for treating type 2 diabetes (Jiang, 2008).To consider other nutritional therapies, Taurine was recognized as the therapeutic agent involved in the development and protection of insulin apparatus because they both have mutual stimulating actions with hypoglycemic properties. Hence, taurine supplementation may be beneficial in treating type 2 diabetes (Kim, Gupta, & Lee, 2007).

Similarly, cereal Oat (Avena sativa) is also believed to be a potential candidate for metabolic disorders like diabetes due to its multifunctional characteristics and nutritional profile.

Oat is a good source of dietary fiber especially beta-glucan, whose different physiological effects are related to its viscosity, attenuation of postprandial plasma glucose, and insulin responses (Sadiq Butt et al., 2008). Therefore, the use of oat grains and oat bran in food products might improve nutrition strategies with therapeutic potential against type 2 diabetes.

Further, to better explore treatment strategies there is also a need to focus on the immunological activity in the episode of type 2 diabetes mellitus. It was reported that Latent autoimmune diabetes in adults (LADA) is clinically similar to type 2diabetes. This disorder could be best classified by the determination of autoantibodies such as glutamic acid decarboxylase (GADA) and Islet cell antibodies (ICA) (Abiru et al., 1996). Seissler (2008) reported that nearly 10% of patients with the clinical characteristics of type 2 diabetes suffer from this autoimmune form of diabetes associated with a rapid decline of residual beta-cell mass and subsequent development of insulin dependency. To ensure the successful treatment to type 2 diabetes there is also a need to focus on this subtype.

It was suggested that all patients should be tested for pancreatic islet autoantibodies during diagnosis of diabetes to facilitate correct diagnosis and to eliminate future failure of hypoglycemic agents and risk of complications due to hyperglycemia (Landin-Olsson, 2002). Hence, this would support an earlier description that mentioned that determining Islet cell antibodies (ICAs), hypogastric antibodies, and Human leukocyte antigens (HLA-DR) would help in characterizing type 2 diabetes (Groop et al., 1988).

Inflammation was considered as another possible risk factor known to contribute to the development of insulin resistance and type 2 diabetes mellitus (Greenfield & Campbell, 2006). This study has further highlighted that elevated levels of circulating acute-phase inflammatory marker, typified by C-reactive protein (CRP) could not only help in understanding the development of obesity about type 2 diabetes but also the mechanisms linking body fat and insulin resistance including the possible role of the toll-like family of immune receptors.

Since inflammation is involved in diabetic patients it may also reveal other associated complications. This is because it was reported that inflammatory marker C-reactive protein (CRP) was strongly believed to predict the risk of coronary heart disease (CHD) (Bahceci et al., 2005). Their research has found similar CRP levels in diabetic patients compared to CRP levels found in non –diabetic patients with CHD.

Therefore, it may indicate that high CRP levels in type 2 diabetic patients might contribute to the same risk that would be prevalent in CHD patients. Hence, it may appear reasonable to infer that CRP levels should be considered cautiously without fail while looking for different treatment strategies for type 2 diabetic patients. The additional insights in the immunological context are about chronic inflammation that is regulated by a special class of biochemical signal molecules called cytokines. In type 2 diabetes, it was reported that the balance between proinflammatory and anti-inflammatory cytokines is shifted toward proinflammation that could potentially cause or aggravate the health complications found in this disorder (Guest et al., 2008).

Over-nutrition has been shown to elicit the innate immune system but activation of the innate immune system itself was found to induce hyperglycemia and insulin resistance. It indicates that diabetes and chronic inflammation are inseparable and act as a reciprocal feed-forward loop (Guest et al., 2008). Hence, it may indicate a defect in cytokine and nutrition regulation.

Previous workers described the involvement of islet cell autoimmunity in the episode of type 2 diabetes mellitus and its connection with acute-phase response protein known as CRP (Pietropaolo et al., 2000). This study has indicated that this association might be responsible for the defect in insulin secretion. Therefore, it can be inferred that this pathogenic link may have future directions for the classification and treatment of diabetes in the elderly and might enable a better understanding of the autoimmune/inflammatory mechanisms involved in the pathogenesis of hyperglycemia. This information may serve as an indispensable tool for developing novel immunotherapeutic approaches.

Prakash, Chenniah, and Murthy (2006) reported an association between type 2 diabetes mellitus and cell-mediated immunological disturbances of T- lymphocyte origin that has a link with insulin defect. They suggested that an enzyme, adenosine deaminase (ADA) could better serve as a marker to assess immunological defects in diabetic patients. This is because adenosine deaminase was considered an as good marker of cell-mediated immunity with its highest activity in T- lymphocytes and its elevated levels were thought to reflect an immunological aberration.

Therefore, it may indicate that markers are important for metabolic disorders like type 2 diabetes mellitus as they not only help in predicting the clinical status but also assist in designing appropriate therapeutic regimens. Hence, immunological research may be considered as the key to understand the pathways behind the clinical conditions and could guide the therapy for patients with type 2 diabetes mellitus.

The other therapeutic approach that needs evaluation is genetic engineering. This branch has drawn the attention of many medical scientists and for long period research has been in progress to provide efficient remedy to individuals suffering from type 2 diabetes.

It is well known that genes are considered as the functional units of inheritance. As such they have the potential to regulate complex biochemical or metabolic pathways that may be essential in maintaining normal homeostasis. A functional defect in these candidates may also lead to abnormalities which could be corrected by genetic engineering or gene therapy. To this end, previous workers have indicated that the gene therapy for type 2 diabetes mellitus could be helpful for the treatment and prevention of the underlying causes of the obesity and insulin resistance (Giannakakos, Pietropaolo & Trucco, 2002).

This was further strengthened by another report. Hansen (2003) highlighted that mutations in insulin receptor gene would cause syndromes of severe insulin resistance and mutations in pancreatic beta-cell genes would cause monogenic sub-group of type 2 diabetes known as maturity-onset-diabetes-of-the-young, MODY. Theses genes were better regarded as “Diabetogenes” by researchers. There is a need to know much about these genes that would be selected and analyzed by the process of candidate gene approach for the treatment of diabetes.

Recombinant DNA technology is a similar process of identifying the desired gene.

Mc Keage and Goa (2001) described that Insulin glargine is a recombinant human insulin analogue produced by DNA technology using a nonpathogenic strain of Escherichia coli.

It has the potential to reduce glycosylated haemoglobin levels. In addition to insulin therapy, it would be useful to establish basal glycaemic control with a single administration per day and a reduced risk of nocturnal hypoglycaemia in patients with type 2 diabetes. Hence, the Insulin glargine therapy must be instituted properly to lessen the incidence of diabetes. The complexity involved for type 2 diabetes is that it requires a better understanding of the processes that determine insulin sensitivity (Giannoukakis & Robbins, 2002).

Therefore, it was reported that targeting tissues such as muscle and fat with vector encoding genes whose products promote insulin sensitivity and glucose uptake is a reliable approach. The other benefit is that it does not induce side-effects often associated with pharmacologic agents (Giannoukakis & Robbins, 2002). A recent report has described that chronic hyperglycaemia that is common to both type 1 and type 2 diabetes could be managed by daily protein treatments (Harrison, 2008).

Therefore, this study has reported that delivery of a single protein using a virus vector could restore euglycaemia in vivo. Hence, this might further strengthen the potential implications of gene therapy or gene based medicine.

The next important aspect to consider is hormone replacement therapy (HRT). It was reported that women who reach postmenopausal stage may suffer from complications like osteoporeosis and cardiovascular diseases in addition to type 2 diabetes mellitus. For this purpose, hormone estrogen was recommended as it could improve the regulation of carbohydrate metabolism, including insulin resistance (Cefalu, 2001).Hence, it may indicate that hormone replacement therapy with estrogen would be beneficial for women with type 2 diabetes and other associated abnormalities. But this study may require further confirmations.

Newton et al. (2003) described that estrogen therapy, with or without another hormone progestin, was associated with the decreased risk of cardiovascular events among women with type 2 diabetes, thus further strengthening the previous study. Honisett Suzy et al. (2004 reported that type 2 diabetes and ovarian senescence are associated with impaired endothelial function in addition to cardiovascular disease. They mentioned that the addition of hormone therapy to thiazolidinediones such as rosiglitazone eliminates or corrects the endothelial dysfunction without altering other cardiovascular risk factors.

Therefore this report has cautioned the use of hormone therapy with thiazolidinedione. On the other hand, hormone therapy also plays beneficial role in men. It was reported that testosterone was found to improve glucose homeostasis and body composition (decrease in visceral obesity) in type 2 diabetic men who have other complaints like symptoms of androgen deficiency.

So, the above two studies may indicate the efficacy of hormone therapy aimed at alleviating type 2 diabetic symptoms and other associated illnesses.

The next focus is on the supplementation of vitamins C and E in combination with hormone replacement therapy as they were believed to strengthen the antioxidant defense system due

to their reducing action on blood glucose and lipid metabolites; and hence may play a role in preventing cardiovascular diseases in postmenopausal women with Type 2 diabetes (Naziroğlu et al., 2004). Further, a recent report has emphasized the role of the liver secreted hormone fetuin –A in inducing insulin resistance in humans (Stefan, 2008). It was considered to be associated with increased plasma glucose levels, thus suggesting its contribution as an independent risk factor of type 2 diabetes.

Since type 2 diabetes mellitus is reported to be associated with a syndrome of risk factors especially of cardiovascular origin, there is need for its early recognition and treatment.

For this purpose, a comprehensive management plan was devised to ensure effective control of this disorder. This is called as “ABCDE” approach. A” for assessment of cardiovascular risk and aspirin therapy, “B” for blood pressure control, “C” for cholesterol management, “D” for diabetes prevention and diet therapy, and “E” for exercise therapy (Blaha et al., 2008). This approach may be reliable in providing a practical and systematic framework for encouraging metabolic syndrome recognition and for implementing a comprehensive, evidence-based management plan for the reduction of cardiovascular risk in patients with type 2 diabetes mellitus.


Type 2 diabetes is one of the severe health problems affecting individuals at an alarming rate. It has been contending with its counter part type1 in inducing the abnormalities that alter the normal levels of glucose. Various therapeutic approaches have been devised to counteract the ill effects of this disorder and they required the applications of different life science branches as shown in table 1.

This has commenced with targeting the life style where diet and exercise were considered to play vital role especially for obese people. Hence, it is obvious from this description that treatments to reduce weight loss were implemented with certain weight reducing agents such as serotonin- and noradrenaline-reuptake inhibitor sibutramine, orlistat, beta3-agonists and drugs such as repaglinide, troglitazone, rosiglitazone etc.

As insulin resistance is the major contributor of type 2 diabetes, oral administration of insulin employing secretagogues and sensitizers has proven to be beneficial. This may be because of their heterogeneous mode of action and efficacy in maintaining long-term glycaemic control for over weight or obese patients in combination with insulin therapy (Krentz & Bailey, 1999). Oral therapy with glucagon-like peptide-1 (GLP-1) inhibitors such as sitagliptin and vildagliptin is another effective strategy aimed at treating type 2 diabetes (Penfornis, Borot and Raccah, 2008).

Further, since glucagon-like peptide-1 is considered as intestinal incretin hormone and has control over glucose homeostasis and insulin secretion, it may find better opportunities in therapeutic applications, which was obvious with Exenatide. Therapy involving repaglinide and metformin or rosiglitazone has indicated that combinational therapy has also good implications for patients with type 2 diabetes. Therefore the above mentioned approaches may appear reliable and could warrant the potential applications of more number of oral antidiabetic drugs aimed at reducing the risk of type 2 diabetes shortly.

However, inspite of some progress achieved in restoring the health of type 2 diabetic patients, concerns do exist particularly about insulin therapy in some sections of the society regarding the selection and this may be eliminated with general awareness and education. Very often patients on insulin therapy may not be benefited and hence might require substitutes or adjuncts like Pramlintide. This approach of adjunctive therapy might appear promising for patients who face problems with conventional drugs. However, the above mentioned drugs may induce side effects and may require long term monitoring.

Next, the approach found to be the most reliable with no adverse affects is Nutrition.

Taurine exerts a beneficial mutual relationship with the insulin apparatus (Villareal et al., 2008).Oat lessens the postprandial plasma glucose and insulin responses (Sadiq Butt et al., 2008). Hence, it may indicate that both the nutritional supplements might play key role in lessening the incidence of type 2 diabetes and may further suggest their incorporation in the daily dietary recipe.

Immunotherapeutic approach may involve prior focus on autoimmunity. This may be due to the detection of autoantibodies to glutamic acid decarboxylase and islet cells of pancreas (Landin-Olsson, 2002). Then, it is the inflammation to consider as the potential risk factor that could be reflected by elevated CRP levels, especially in type 2 diabetic patients with associated cardiovascular problems (Greenfield & Campbell, 2006). Further, abnormal

T- lymphocyte function interlinked with insulin defect could be better evaluated by markers like adenosine deaminase in type 2 diabetic patients (Prakash, Chenniah, & Murthy, 2006).Genetic approach has led to the finding of sub-group of type 2 diabetes known as maturity-onset-diabetes-of-the-young (Hansen ,2003). Therefore gene therapy was strongly indicated as another treatment option (Giannoukakis, Pietropaolo & Trucco, 2002).Insulin glargine is a recombinant human insulin with better therapeutic implications (Mc Keage & Goa, 2001). Hormone therapy with estrogen and testosterone undecanoate may not only improve the diabetic condition of the patients but also other related symptoms. Hence, its implementation is a must in clinics.


The metabolic disorder type 2 diabetes mellitus has different treatment methods because of the diversity involved in the manifestation of symptoms in association with obesity, cardiovascular disease, and postmenopausal problems. Several approaches have been recommended and targeted overweight or obese patients. Oral therapy that involves Thiazolidinediones with other agents in a combinational approach may better address the problems of type 2 diabetic patients. Adjunctive therapy would help in choosing treatment other than insulin.

Nutritional approach may be considered comparatively safe with supplements like taurin, oat, and vitamins C and E. Malfunction of immunological parameters has prompted to evaluate autoantibodies, inflammatory mechanisms and T- lymphocyte dysfunction. This may be due to the problem of autoimmunity, cardiovascular problems and other age related complications. This has ultimately led to the necessity of markers like C- reactive protein and adenosine deaminase that were believed to assess the clinical status and treatment efficacy. This has implied that type 2 diabetes is having strong immunological etiology.

Hence, immunotherapeutic evaluation may furnish better insights regarding the pathogenesis and might assist in designing novel drugs. The recent ABCDE approach may help in better evaluating cardiviovasular problems in patients with type2 diabetes. Genetic engineering or Recombinant DNA technology has also made significant contribution in finding “Diabetogenes” and “Insulin glargine”. Given the this concluding description it is reasonable to state that a spectrum of treatment approaches are made available to

circumvent the risk contributing factors of type 2 diabetes mellitus. To choose the best treatment option, thinking from broad perspective with awareness and education are suggestive. However, for better confirmation additional studies may be required.


  1. Abiru, N., Takino, H., Yano, M., Kawasaki, E., Yamasaki, H., Yamaguchi, Y., Akazawa, S., Nagataki, S. (1996). Clinical evaluation of non-insulin-dependent diabetes mellitus patients with autoantibodies to glutamic acid decarboxylase. J Autoimmun, 9, 683-8.
  2. Bahceci, M., Tuzcu, A., Ogun, C., Canoruc, N., Iltimur, K., Aslan, C. (2005). Is serum C-reactive protein concentration correlated with HbA1c and insulin resistance in Type 2 diabetic men with or without coronary heart disease? J Endocrinol Invest, 28, 145-50.
  3. Blaha, M.J., Bansal, S., Rouf, R., Golden, S.H., Blumenthal, R.S., Defilippis, A.P. (2008). A practical “ABCDE” approach to the metabolic syndrome. Mayo Clin Proc, 83, 932-41.
  4. Cefalu, W.T. (2001). The use of hormone replacement therapy in postmenopausal women with type 2 diabetes. J Womens Health Gend Based Med, 10, 241-55.
  5. Edelman, S.V. (1998). Type II diabetes mellitus. Adv Intern Med, 43, 449-500.
  6. Edelman, S.V & Weyer, C. (2002). Unresolved challenges with insulin therapy in type 1 and type 2 diabetes: potential benefit of replacing amylin, a second beta-cell hormone. Diabetes Technol Ther, 4, 190-2.
  7. Giannoukakis, N., Pietropaolo, M., Trucco, M. (2002). Genes and engineered cells as drugs for type I and type II diabetes mellitus therapy and prevention. Curr Opin Investig Drugs, 3, 735-51.
  8. Giannoukakis, N and Robbins, P.D. (2002). Gene and cell therapies for diabetes mellitus: strategies and clinical potential. Bio Drugs, 16, 149-73.
  9. Greenfield, J.R and Campbell, L.V (2006). Relationship between inflammation, insulin resistance and type 2 diabetes: ’cause or effect’? Curr Diabetes Rev, 2, 195-211.
  10. Groop, L, Miettinen, A, Groop, P.H., Meri, S., Koskimies, S., Bottazzo, G.F. (1988). Islet cell antibodies (ICAs), thyrogastric antibodies, and HLA-DR antigens. Diabetes, 37, 99-103.
  11. Guerci, B and Martin, C.S. (2008). Exenatide: its position in the treatment of type 2 diabetes. Ann Endocrinol (Paris), 69, 201-9.
  12. Guest, C.B., Park, M.J., Johnson, D.R., Freund, G.G. (2008). The implication of proinflammatory cytokines in type 2 diabetes. Front Biosci, 13, 5187-94.
  13. Hansen L. (2003).Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility genes or common polymorphisms? Dan Med Bull, 50, 320-46.
  14. Harrison, P.T. (2008).Application of gene therapy in diabetes care. Infect Disord Drug Targets, 8, 129-33.
  15. Honisett Suzy, Y, Stojanovska Lily, Sudhir Krishnankutty, Kingwell Bronwyn, A, Dawood Tye, Komesaroff Paul, A. (2004). Hormone therapy impairs endothelial function in postmenopausal women with type 2 diabetes mellitus treated with Rosiglitazone. The Journal of clinical endocrinology and metabolism, 89, 4615-4619.
  16. Jiang, W.J. (2008). Sirtuins: novel targets for metabolic disease in drug development. Biochem Biophys Res Commun, 373, 341-4.
  17. Kim, S.J., Gupta, R.C., Lee, H.W. (2007). Taurine-diabetes interaction: from involvement to protection. Curr Diabetes Rev, 3, 165-75.
  18. Krentz, A.J & Bailey, C.J (2005).Oral antidiabetic agents: current role in type 2 diabetes mellitus. Drugs, 65,385-411.
  19. Landin-Olsson, M. (2002). Latent autoimmune diabetes in adults. Ann N Y Acad Sci, 958, 112-6.
  20. Levy P. Insulin analogs or premixed insulin analogs in combination with oral agents for treatment of type 2 diabetes. MedGenMed, 9, 12.
  21. McKeage, K and Goa, K.L. (2001). Insulin glargine: a review of its therapeutic use as a long-acting agent for the management of type 1 and 2 diabetes mellitus. Drugs, 61, 1599-624.
  22. Mudaliar, S and Edelman, S.V. (2001). Insulin therapy in type 2 diabetes. Endocrinol Metab Clin North Am, 30, 935-82.
  23. Mudaliar, S. (2007). New frontiers in the management of type 2 diabetes. Indian J Med Res, 125, 275-96.
  24. Naziroğlu, M., Simşek, M., Simşek, H., Aydilek, N., Ozcan, Z., Atilgan, R. (2004). The effects of hormone replacement therapy combined with vitamins C and E on antioxidants levels and lipid profiles in postmenopausal women with Type 2 diabetes. Clin Chim Acta, 344, 63-71.
  25. Newton, K.M., LaCroix, A.Z., Heckbert, S.R., Abraham, L., McCulloch, D., Barlow, W. (2003). Estrogen therapy and risk of cardiovascular events among women with type 2 diabetes. Diabetes Care, 26, 2947-58.
  26. Penfornis, A, Borot S, Raccah D. Therapeutic approach of type 2 diabetes mellitus with GLP-1 based therapies. Diabetes Metab. 34, S78-90.
  27. Pietropaolo, M., Barinas-Mitchell, E, Pietropaolo, S.L., Kuller, L.H., Trucco, M. (2000). Evidence of islet cell autoimmunity in elderly patients with type 2 diabetes. Diabetes, 49, 32-8.
  28. Plosker, G.L & Figgitt, D.P. (2004). Repaglinide: a pharmacoeconomic review of its use in type 2 diabetes mellitus. Pharmacoeconomics, 22, 389-411.
  29. Reasner, C.A.2nd. (1999). Promising new approaches. Diabetes Obes Metab, 1, S41-8.
  30. Sadiq Butt, M., Tahir-Nadeem, M., Khan, M.K., Shabir, R., Butt, M.S. (2008). Oat: unique among the cereals. Eur J Nutr, 47, 68-79.
  31. Seissler, J. (2008). Latent (slowly progressing) autoimmune diabetes in adults. Curr Diab Rep, 8, 94-100.
  32. Shiva Prakash, M., Chennaiah, S, Murthy, Y.S.R., Anjaiah, E, Ananda Rao, S., Suresh, C.(2006).Altered Adenosine deaminase activity in type 2 diabetes mellitus. JIACM, 7, 114-7.
  33. Stefan, N., Fritsche, A, Weikert, C., Boeing, H., Joost, H.G., Häring, H.U., Schulze, M.B. (2008). Plasma Fetuin-A Levels and the Risk of Type 2 Diabetes. Diabetes. [Epub ahead of print] Web.
  34. Stonehouse, A.H., Holcombe, J.H., Kendall, D.M. (2006). Management of Type 2 diabetes: the role of incretin mimetics. Expert Opin Pharmacother 7, 2095-105.
  35. Steyn, N.P., Mann, J., Bennett, P.H., Temple, N., Zimmet, P., Tuomilehto, J., Lindström, J., Louheranta, A. (2006).Diet, nutrition and the prevention of type 2 diabetes. Public Health Nutr, 9,276.
  36. Villareal, D.T., Banks, M.R., Patterson, B.W., Polonsky, K.S., Klein, S. (2008). Weight loss therapy improves pancreatic endocrine function in obese older adults. Obesity (Silver Spring), 16, 1349-54.

Table 1. Therapeutic Applications of different life science braches for type 2 diabetes mellitus

Branch Applications
1.Biochemistry Weight reduction therapy
2.Nutrition Therapy involving supplementation of taurine, oat, vitamins
3. Immunology Evaluation of markers, C-reactive protein and Adenosine deaminase.
4.Genetics or Recombinant DNA technology Gene therapy
5.Endocrinology Hormone replacement therapy
6. Pharmacology Drugs (repaglinide, rosiglitazone, etc)
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