Mechanism
Diphtheria toxin (DT) is produced only by C. diphtheriae infected with a certain type of bacteriophage. Toxinogenicity is determined by phage conversion (also called lysogenic conversion); i.e, the ability of the bacterium to make DT changes as a consequence of infection by a particular phage. DT is encoded by the tox gene. Strains of corynephage are either tox+ (e.g., corynephage β) or tox- (e.g., corynephage γ). The tox gene becomes integrated into the bacterial genome. The chromosome of C. diphtheriae has two different but functionally equivalent bacterial attachment sites (attB) for integration of β prophage into the chromosome. Diphtheria toxin precursor is a protein of molecular weight 60 kDa. Certain proteases, such as trypsin, selectively cleave DT to generate two peptide chains, amino-terminal fragment A (DT-A) and carboxyl-terminal fragment B (DT-B), which are held together by a disulfide bond. DT-B is a recognition subunit that gains entry of DT into the host cell by binding to the EGF-like domain of heparin-binding EGF-like growth factor  on the cell surface. This signals the cell to internalize the toxin within an endosome via receptor-mediated endocytosis. Inside the endosome, DT is split by a trypsin-like protease into DT-A and DT-B. The acidity of the endosome causes DT-B to create pores in the endosome membrane, thereby catalysing the release of DT-A into the cytoplasm.Fragment A inhibits the synthesis of new proteins in the affected cell by catalyzing ADP-ribosylation of elongation factor EF-2—a protein that is essential to the translation step of protein synthesis.
Such symptoms include:
Increased thirst
Increased urination, especially waking up in the night to urinate
Tiredness and fatigue
Blurred vision
Slow healing of wounds
Altered sensation, such as numbness or tingling, particularly of the hands and feet
Recurrent, and difficult to clear infections, particularly of the urinary tract

Risk factors
As impaired fasting glucose is considered a precursor condition for type 2 diabetes, it shares the same environmental and genetic risk factors. Diagnosis
Different organisations use slightly differing levels before classifying a persons fasting blood glucose as "impaired", with the American Diabetes Association using a lower cutoff in its criteria than the World Health Organization. The upper limits remain the same, as fasting levels above this are almost universally accepted as indicative of full diabetes:

WHO criteria: fasting plasma glucose level from 6.1 mmol/L (110 mg/dL) to 6.9 mmol/L (125 mg/dL). ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL). Prevention
The guidelines for preventing impaired fasting glucose are the same as those given for preventing type 2 diabetes in general. If these are adhered to, the progression to clinical diabetes can be slowed or halted. In some cases, a complete reversal of IFG can be achieved. Certain risk factors, such as being of Afro-Caribbean or South Asian ethnicity, as well as increasing age, are unavoidable, and such individuals may be advised to follow these guidelines, as well as monitor their blood glucose levels, more closely. Management
References


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