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Role Of Inflammation And Oxidative Stress In Development Of Type 2 Diabetes Without Family History

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The emergence of Type 2 Diabetes Mellitus [T2DM] as a pandemic is one of the major challenges to human health in 21st century [1]. Diabetes is currently ranked 9th in the world among the leading causes of death [2]. Globally, the incidence of Diabetes mellitus is increasing in all age groups. The prevalence was estimated to be around 2.8% in 2000, while recent trends show that it might increase to 4.4% by 2030 [3]. Research In the past few years has linked oxidative stress and inflammation to β-cell dysfunction [4]. Besides, inflammation and oxidative stress are deeply inter-related and are known to play an important role in development of its vascular complications [5].

T2DM has been classified as chronic inflammatory state with evidence of increased levels of cytokines and acute phase reactants [6]. This chronic low grade inflammatory response along with activation of innate immune system has been associated with development of DM [7]. hs-CRP is an acute phase reactant produced by liver. It is considered to be a major inflammatory mediator that functions as a non-specific defence mechanism in response to tissue injury or infection. Recent studies have shown that an elevated level of CRP is associated with an increased risk of developing T2DM [8,9].

Similarly, increased oxidative stress leads to accumulation of Reactive Oxygen Species (ROS) and cause activation of stress-sensitive intracellular signalling pathways. This inturn promote cellular damage and contribute to the development of Diabetes and its progression [10].

GGT is a cell surface protein which is responsible for extracellular catabolism of glutathione (GSH). GGT has been well recognized as a marker of oxidative stress [11]. Recent studies indicated that high level of GGT is associated with pathogenesis of diabetes [12,13].

Besides family history is an important non-modifiable risk factor for development of diabetes. It is a disease which has a strong clustering in families and has a genetic component [14]. The association between family history and development of diabetes is well documented [15,16]. The risk of T2DM increases by about 2-4 fold when one or both parents are affected [17,18].

However, there are limited studies linking both oxidative stress and family history in development of diabetes mellitus. In view of the above, the present study was planned in newly diagnosed T2DM patients taking family history into consideration.


The main objectives of the present study is to-

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  • (a) Measure Inflammatory marker (hs-CRP) and oxidative stress marker (GGT) in newly diagnosed T2DM patients with family history of type 2 diabetes.
  • (b) Measure inflammatory marker (hs-CRP) and oxidative stress marker (GGT) in newly diagnosed T2DM patients without family history of type 2 diabetes.
  • (c) Compare the above markers in both the groups.
  • (d) Correlate the values of above markers with FBS, PPBS values in both groups, to know the extent of relation between the variables.


  • (i) Study Design: This will be a cross-sectional study planned in GSL Medical College/General Hospital, Rajamahendravaram, AP.
  • (ii) Study Area: The study will be conducted among the patients attending Medicine OP, GSL General Hospital and subsequently diagnosed with T2DM based on investigations done in Central lab, Department of Biochemistry, GSL General Hospital.
  • (iii) Study subjects: A total of 60 patients of newly diagnosed T2DM between 30-60 yrs, both males & females will be involved in the study. They will be divided into 2 following groups:

Group 1: 30 patients of T2DM with family history of type2 diabetes.

Group 2: 30 patients of T2DM without family history of type 2 diabetes.

  • (a) Inclusion criteria: Patients in age group of 30-60 yrs and newly diagnosed with T2DM according to ADA criteria (FBS > 126 mg/dl & PPBS > 200mg/dl)
  • (b) Exclusion criteria: (1) Old cases of T2DM

(2) Pregnant women, hypertensives, alcoholics, smokers and on medications like steroids, vitamin supplements, NSAID’s etc.

(3) Patients with immunological disorders, inflammatory disorders, liver diseases and any other co-morbid conditions

  • (iv) Ethical approval & Informed consent: Ethical approval will be obtained from the Institutional Ethical Committee before the start of the study. Informed consent will be obtained from the study subjects before data & blood sample collection.
  • (v) Co-variables: In the present planned study co-variables include age, gender, diet, smoking, alcohol, family history etc. The above information will be collected from all the subjects using a simple questionnaire. Family history will be taken as positive if any first degree relative of the patient had T2DM.
  • (vi) Estimation of biochemical markers: The following parameters will be estimated in serum obtained from the blood sample drawn from study subjects.

(1) Fasting blood sugar (FBS) (2) Post prandial blood sugar (PPBS)

(3) Inflammatory marker-hsCRP (4) Oxidative stress marker-GGT

  • (vii) Statistical analysis: SPSS software will be used. The variables will be expressed as mean+SD using student t-test. Correlation between the variables will be assessed by Pearson’s correlation coefficient.


There are several evidences which provided extensive literature about the role of inflammation and oxidative stress in T2DM. However there are limited studies which compared these markers taking family history as criteria. Besides, the effect of duration on these biomarkers was not considered in many previous studies. Hence the present study was planned addressing the above concerns by taking family history as criteria and selecting only newly diagnosed cases. This may add more evidences to the current literature, associating, inflammatory and oxidative stress in development of T2DM with no family history of diabetes.

hs-CRP may be a non-specific marker but when combined with oxidative stress marker like GGT, may fulfil the objectives of the study. Measurement of these biomarkers in serum is reliable, easy and inexpensive. The activity of GGT in serum is also highly stable. Besides, monitoring these markers along with blood glucose levels at regular intervals may provide valuable information regarding the progression of the disease and development of vascular complications.


  1. IDF Diabetes atlas, 7th Ed. Brussels, Belgium. International diabetes federation, 2015.
  2. Jalkrit Bhutani, Sukruti Bhutani. Worldwide burden of diabetes. Ind J of endocrinology and metabolism, 2018; vol.18: 2-4.
  3. Chan JC, Malik V, Jia, Kadowaki, Yagnik CS et al. Diabetes in Asia: Epidemiology, risk factors & Pathophysiology. JAMA. 2009; 301:2129-2140.
  4. Karp DR, Shimooku K, Lipsky PE. Expression of GGT protects rumos b-cells from oxidation induced cell death. J Biol chem. 2001; 12: 3798-3804.
  5. Hojs R, Ekart R, Bevc S, Hojs N. Markers of inflammation and oxidative stress in the development and progression of renal disease in diabetic patients. Nephron.2016; 286:327-34.
  6. Dallmeier D, Larson MG, Vasan RS et al. Metabolic syndrome and inflammatory biomarkers: A community based cross-sectional study at the Framingham heart study. Diabetol met syn.2012; 4:28-34.
  7. Esposito K, Giugliano D. The metabolic syndrome & inflammation: association or causation? Nutr metab cardiovasc dis.2004; 14(5):228-32
  8. Pradhan AD, Manson JE, Rifai N et al. CRP, IL-6 and risk of developing type 2 diabetes mellitus. J Am med assoc.2001; 286:327-34.
  9. Thorand B, Lowel H, Schneider A et al. CRP as predictor for incident diabetes mellitus among middle aged men. Arch Intern med.2003; 16:93-99.
  10. Maritim AC, Sanders A, Watkins J. Diabetes, oxidative stress and anti oxidants: A review. Jour of Biochem & mol. toxicology.2003; 17(1):24-38.
  11. Pleiner J, Mittermayer F, Schaller G et al. Inflammation induced vasoconstrictor hyporeactivity is caused by oxidative stress. J Am coll cardiol 2003; 42:1656-62
  12. Lee DH, Jacobs DR, Gross M et al. GGT is a predictor of incident diabetes and hypertension: the coronary artery risk development in young adults (CARDIA) study. Clin chem 2003; 49:1358-66.
  13. Nakanishi N, Suzuki K, Tatara K. Serum GGT & risk of metabolic syndrome and type 2 diabetes in middle-aged Japanese men. Diabetes care 2004; 27:1427-32.
  14. Ramachandran A. Epidemiology of type 2 diabetes in India. J.Indian med.assoc. 2002; 100: 425-27.
  15. Harrison TA, Hindroff LA, Kim H et al. Family history of diabetes as a potential public health tool. Am J prev med 2003; 24:152-159.
  16. Meigs JB, Cupples LA, Wilson PW. Parental transmission of type 2 diabetes: the Framingham offspring study. Diabetes 2000; 49:2201-2207.
  17. Klein BE, Klein R, Moss SE et al. Parental history of diabetes in a population based study. Diabetes care 1996; 19(8):827-30.
  18. Alcolado JC, Alcolado R. Imp of maternal history in non-insulin dependent diabetic patients. BMJ 1991; 302:1178-80.

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Role Of Inflammation And Oxidative Stress In Development Of Type 2 Diabetes Without Family History. (2022, February 17). Edubirdie. Retrieved March 31, 2023, from
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