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J R Soc Med 2004;97:511-520
doi:10.1258/jrsm.97.11.511
© 2004 Royal Society of Medicine

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Metabolic syndrome: maladaptation to a modern world

Terence J Wilkin MD FRCP     Linda D Voss PhD  

Department of Endocrinology & Metabolism, Peninsula Medical School (Plymouth campus), Level 7, Derriford Hospital, Plymouth PL6 8DH, UK



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  		Figure 1. The shift in distribution of BMI of UK adults between the 1970s (black) and the 1990s (open).

Both the median and the mean have moved, suggesting that the whole of society is involved. Modified from ref. 3

 


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  		Figure 2. Schematic representation of the feedback loop controlling blood glucose.

If the islets fail (type 1 diabetes), glucose rises because insulin falls. If the tissues fail (type 2 diabetes), insulin rises because glucose rises

 


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  		Figure 3. The metabolic wheel. Insulin resistance at its centre simultaneously drives a number of metabolic processes. The spokes are each linked through the hub, rather than to each other. PAI-1=plasminogen activator inhibitor 1; PCV=haematocrit

 


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  		Figure 4. A transverse abdominal CT scan showing intraabdominal visceral fat in black (area 13459 mm2, metabolically harmful) but, in addition, a substantial amount of subcutaneous fat (area 5823 mm2, metabolically harmless)

 


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  		Figure 5. The relationship between visceral adiposity (% central abdominal fat), BMI and insulin resistance. BMI does not inform on fat distribution and is a poor proxy for insulin resistance (After Ref. 47)

 

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