A followup to my original post stating that thin people can be T2 diabetic.
The link doesn't look like it's wrapping to me, so I've posted the abstract
below.
http://diabetes.diabetesjournals.org/cgi/content/abstract/47/5/699?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&andorexacttitle=and&titleabstract=normal+weight&andorexacttitleabs=phrase&andorexactfulltext=and&searchid=1084764548662_2983&stored_search=&FIRSTINDEX=0&sortspec=relevance&journalcode=diabetes&journalcode=diaclin&journalcode=diacare&journalcode=diaspect
Comparable articles can be found at
http://diabetes.diabetesjournals.org/

ABSTRACT:
The metabolically obese, normal-weight individual revisited
N Ruderman, D Chisholm, X Pi-Sunyer and S Schneider
Evans Department of Medicine, Boston University Medical Center,
Massachusetts 02118, USA. [log in to unmask]

Nearly 20 years ago, it was suggested that individuals exist who are not
obese on the basis of height and weight, but who, like people with overt
obesity, are hyperinsulinemic, insulin-resistant, and predisposed to type 2
diabetes, hypertriglyceridemia, and premature coronary heart disease. Since
then it has become increasingly clear that such metabolically obese,
normal-weight (MONW) individuals are very common in the general population
and that they probably represent one end of the spectrum of people with the
insulin resistance syndrome. Available evidence also suggests that MONW
individuals could account for the higher prevalence of type 2 diabetes,
cardiovascular disease, and other disorders in people with a BMI in the
20-27 kg/m2 range who have gained modest amounts of weight (2-10 kg of
adipose mass) in adult life. Specific factors that appear to predispose
MONW, as well as more obese individuals, to insulin resistance include
central fat distribution, inactivity, and a low VO2max. Because these
factors are potentially reversible and because insulin resistance may
contribute to the pathogenesis of many diseases, it is our premise that a
compelling argument can be made for identifying MONW individuals and
treating them with diet, exercise, and possibly pharmacological agents
before these diseases become overt, or at least early after their onset. One
reason for doing so is that disorders such as type 2 diabetes may be
accompanied by irreversible consequences, e.g., ischemic heart disease and
nephropathy, at the time of diagnosis or shortly thereafter. Another is that
MONW individuals in general should be younger and more amenable and
responsive to diet and exercise therapy than are obese patients with
established disease. That long-term diet and exercise can work is suggested
by two large studies in which, over 5-6 years, the incidence of diabetes was
diminished in nonobese and minimally obese patients with impaired glucose
tolerance. Based on these considerations and the emerging worldwide epidemic
of type 2 diabetes, we believe that studies to assess whether therapies
aimed at young MONW individuals can prevent the development of type 2
diabetes and other diseases, including perhaps obesity itself, are urgently
needed.