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Review
. 2004 Nov;97(11):511-20.
doi: 10.1177/014107680409701102.

Metabolic syndrome: maladaptation to a modern world

Terence J Wilkin  1 , Linda D Voss
Affiliations
Review

Metabolic syndrome: maladaptation to a modern world

Terence J Wilkin et al. J R Soc Med. 2004 Nov.
No abstract available

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Figures

<i>Figure 1</i>
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.
<i>Figure 2</i>
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
<i>Figure 3</i>
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
<i>Figure 4</i>
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)
<i>Figure 5</i>
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)
See this image and copyright information in PMC

Comment in

  • The liver in metabolic syndrome.
    Smith AD. Smith AD. J R Soc Med. 2005 Jul;98(7):336. doi: 10.1177/014107680509800719. J R Soc Med. 2005. PMID: 15994602 Free PMC article. No abstract available.

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