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in Sera of Obese Patients: Fall with Weight Loss
Division of Endocrinology-Diabetes (P.D., K.T., E.A.-R., A.A.), Department of Medicine, Millard Fillmore Health System, State University of New York at Buffalo, Buffalo, New York 14209; Endocrine Unit (R.W.), Department of Medicine, State University of New York at Syracuse, Syracuse, New York 13210; and Department of Psychiatry (T.W.), University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
Address all correspondence and requests for reprints to: Paresh Dandona, Director, Diabetes-Endocrine Center of Western New York, Millard Fillmore Health Systems, 3 Gates Circle, Buffalo, New York 14209.
In view of the recent demonstration that obesity in animals and humans
is associated with an increase in tumor necrosis factor-
(TNF)
expression, that this expression falls with weight loss, and that
TNF may specifically inhibit insulin action, the possibility that
TNF may be a mediator of insulin resistance has been raised. We have
undertaken this study to investigate whether serum TNF
concentrations are elevated in obese subjects, whether they fall after
weight loss, and whether this fall parallels the fall in insulin
release after glucose challenge. Obese patients (age range: 25–54,
weight mean ± SD: 96.4 ± 13.8 kg, body
mass index: 35.7 ± 5.6 kg/m2) were started on a diet
program. The mean weight fell to 84.5 ± 11.3
(P < 0.0001) and body mass index to 31.3 ±
4.9 (P < 0.0001). Plasma TNF concentrations
were markedly elevated in the obese (3.45 ± 0.16 pg/mL), when
compared with controls (0.72 ± 0.28 pg/mL), and fell
significantly (2.63 ± 1.40 pg/mL) after weight loss
(P < 0.02). The magnitude of insulin release after
glucose (75 g) challenge (area under the curve) also fell significantly
(P < 0.01) after weight loss. The magnitude of
weight loss and fall in TNF were related to basal body weight
(r = 0.57, P < 0.001) and basal TNF
(r = 0.55, P < 0.001) concentrations,
respectively, but not to each other or to the glucose-induced insulin
release (area under the curve). We conclude that obesity is associated
with increased plasma TNF concentrations, which fall with weight
loss. Because circulating TNF may mediate insulin resistance in the
obese, a fall in TNF concentrations may contribute to the
restoration of insulin resistance after weight loss, Thus, TNF may
be an important circulating cytokine, which may provide a potentially
reversible mechanism for mediating insulin resistance.
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