We read with interest the article by Alvarez et al, which
aimed to investigate the relations of circulating 25-hydroxyvitamin
D [25(OH)D] and parathyroid hormone (PTH) concentrations with
direct measurements of insulin sensitivity, after robust measures of
body composition and fat distribution were accounted for. We
would like to express our opinion and a different interpretation of
the data provided by authors, with the hope that other points for
discussion are brought up.
In a very recent publication, Alvarez et al provided novel findings
suggesting that dietary vitamin D is independently associated
with insulin sensitivity in African Americans (AAs) but not in European
Americans (EAs). Interestingly, the 2 groups were identical
for hepatic insulin sensitivity [homeostatic model assessment
(HOMA)], whereas Si, a method for measuring insulin sensitivity
that encompasses both hepatic and peripheral tissues, was lower in
AAs, therefore suggesting a pivotal role for insulin resistance in
skeletal muscle [especially in the presence of identical body mass
index (BMI)] in correlation with 25(OH)D. In the present article,
the authors suggest that 25(OH)D and PTH concentrations are independently
associated with whole-body insulin sensitivity and suggest
that these variables may influence insulin sensitivity through
independent mechanisms. In fact, multiple linear regression analysis
indicated that 25(OH)D and PTH concentrations were independently
related to Si after adjustment for age, race, and intraabdominal
adipose tissue. It is well known, however, that adipose tissue is
the natural reservoir for lipo-soluble 25(OH)D. The higher BMI and
the higher subcutaneous fat content found in AAs (although the
latter difference was not statistically significant) could therefore
explain the differences in 25(OH)D concentration, as well as in
HOMA index, found by the authors.
We examined the effect of 25(OH)D on insulin sensitivity in
obese subjects and found a linear correlation between them, which
is apparently in agreement with Alvarez et al. Obesity, however, is
not invariably associated with insulin resistance, because normal insulin
sensitivity can be present in some obese subjects. If 25(OH)D
concentration influences insulin sensitivity independently of obesity,
it should be found to be low in insulin-resistant obese subjects
and high in insulin-sensitive obesity. We divided our obese population
into 2 subgroups, according to their insulin sensitivity (low and
high). The 2 groups were similar in BMI, age, and sex but did not
show any difference in 25(OH)D concentration, thus confirming the
hypothesis that 25(OH)D concentrations are not influenced by the
degree of insulin resistance but mainly by the adipose tissue\u2019s reservoir,
at least in our EA participants. Unfortunately, in the presentstudied
population but not in the previous one, AAs had
higher BMI (and HOMA) and the actual role of these variables in
determining hypovitaminosis D was not ruled out.
In conclusion, we are certain that 25(OH)D concentration mainly reflects
body fatmass, either subcutaneous or visceral; the reduction of fat
mass, rather than vitamin D supplementation, is the best route for
the prevention and treatment of insulin resistance and diabetes