Visceral fat deposition and insulin sensitivity in depressed women with and without comorbid borderline personality disorder.
OBJECTIVE
Major depressive disorder (MDD) is associated with increased intra-abdominal fat, an important antecedent of noninsulin-dependent diabetes mellitus (NIDDM) and cardiovascular disorders. Furthermore, MDD is commonly accompanied by endocrine and immune dysregulation that has also been discussed in connection with the pathogenesis of NIDDM and ischemic heart disease. In borderline personality disorder (BPD), a dysregulation of the hypothalamic-pituitary-adrenal system has also been described. Therefore, our study aimed at examining visceral fat, insulin resistance, and alterations of cortisol and cytokines in young depressed women with and without comorbid BPD.


METHODS
Visceral fat was measured in 18 premenopausal women with MDD and in 18 women comorbid with MDD and BPD by means of magnetic resonance tomography at the level of the first lumbar vertebral body. Twelve BPD patients without MDD and 20 healthy women served as the comparison groups. Concentrations of fasting cortisol, tumor necrosis factor-alpha, and interleukin-6 were measured, and indicators of insulin resistance and beta-cell sensitivity were calculated according to the homeostasis assessment model.


RESULTS
We found increased visceral fat in women comorbid with MDD and BPD, and to a lesser extent, in women with MDD but without BPD. Insulin sensitivity was reduced in comorbid patients. Serum interleukin-6 (IL-6) and tumor necrosis factor-alpha concentrations were significantly increased in both groups of depressed patients. Reduced insulin sensitivity correlated with the amount of visceral fat and with serum concentrations of IL-6.


CONCLUSIONS
Young depressed women with and without comorbid BPD display increased visceral fat and may constitute a risk group for the development of NIDDM and the metabolic syndrome. Our data support the hypothesis that the immune and endocrine alterations associated with MDD and BPD may contribute to the pathophysiologic processes associated with NIDDM.
Kahl
Kai G
KG
Department of Psychiatry and Psychotherapy, University of Luebeck, Germany. kahl.k@psychiatry.uni-luebeck.de
Bester
Maxim
M
Greggersen
Wiebke
W
Rudolf
Sebastian
S
Dibbelt
Leif
L
Stoeckelhuber
Beate M
BM
Gehl
Hans-Björn
HB
Sipos
Valerija
V
Hohagen
Fritz
F
Schweiger
Ulrich
U
D000328:Adult; D001883:Borderline Personality Disorder / Q000097:blood / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D015897:Comorbidity; D003865:Major Depressive Disorder / Q000097:blood / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis / Q000276:immunology / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007333:Insulin Resistance / Q000276:immunology / Q000502:physiology*; D015850:Interleukin-6 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008954:Models, Biological; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose; D006854:Hydrocortisone