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Table 2. WHO and ADA criteria for the diagnosis of diabetes


                             Criteria for the diagnosis of diabetes
           Fasting plasma        ≥126 mg/dl (7.0 mmol/l)
           glucose (FPG)*  (4, 5)
                                           or
           Post-prandial glucose   ≥200 mg/dl (11.1 mmol/l)
           (PPG) *  (4, 5)
                a
                                           or
           HbA 1c b *  (5)       ≥6.5%

                                           or

           Random plasma         ≥200 mg/dl (11.1 mmol/l)
           glucose c (5)

          a   Defined using the 2h oral glucose tolerance test (OGTT) after ingesting the 75g glucose load. 4
          B   The test should be performed in a laboratory using a method that is NGSP certified and stand-
            ardised to the DCCT assay. 5
          c   In a patient with classic symptoms of hyperglycaemia or hyperglycaemic crisis. 5
          *  In the absence of unequivocal hyperglycaemia, FPG, PPG and HbA  should be confirmed by
                                                            1c
            repeat testing.



          Glucose metabolism: an overview

          T2DM is a disease of glucose homeostasis, so it is pertinent here to briefly
          review the basics of glucose metabolism. ATP, the universal energy cur-
          rency of life, is generated via the oxidation of glucose, non-esterified
          fatty acids (NEFA) and, to a lesser extent, amino acids. Glucose can
          be  obtained  from  food  via  digestion  or  it  can  be  synthesised  in  the
          body.  Glucose  obtained  from  carbohydrates  in  the  diet  is  actively
          transported from the lumen of the intestine into the blood by the main
          transporter protein, sodium-glucose transport protein 1 (SGLT-1) 9 10  The
          majority of absorbed glucose reaches the liver where it is in part stored
          as glycogen (glycogen synthesis), whilst the remainder is taken up by
          peripheral tissues for both oxidative and non-oxidative (storage) use;
          excess glucose is converted into lipids (de novo lipogenesis) in the liver
          and, to a lesser degree, in adipose tissue. 11 12










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