Lithium Decreases Plasma Adiponectin Levels in Bipolar Depression
•At baseline, adipokines levels between BD subjects and controls did not differ.•Levels of adiponectin significantly decreased after lithium monotherapy.•Leptin and resistin levels did not change after 6-week lithium treatment.•Pretreatment levels of leptin were higher in remitters.•changes in resis...
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Veröffentlicht in: | Neuroscience letters 2014-04, Vol.564, p.111-114 |
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Zusammenfassung: | •At baseline, adipokines levels between BD subjects and controls did not differ.•Levels of adiponectin significantly decreased after lithium monotherapy.•Leptin and resistin levels did not change after 6-week lithium treatment.•Pretreatment levels of leptin were higher in remitters.•changes in resistin levels were negatively correlated to improvement of depressive symptoms with lithium.
Lithium, a first line treatment for bipolar disorder (BD), has been associated with significant weight gain, but the mechanisms underlying this phenomenon are still unclear. It has been suggested that changes in production/release of adipokines – molecules secreted by adipose tissue presenting anti-inflammatory (adiponectin) and pro-inflammatory (leptin, resistin) properties – might be implicated. Adiponectin, resistin and leptin were assessed in 25 acutely depressed BD individuals (88% medication-free and 68% treatment-naive) at baseline and after 6 weeks of lithium therapy, and in 23 healthy controls matched by age. The 21-item Hamilton Depression Rating Scale was used to assess depression severity. Levels of adiponectin significantly decreased after lithium monotherapy, while the levels of resistin and leptin remained stable after the follow-up period. Adipokine levels during depressive episodes in BD did not differ compared to controls. Pretreatment levels of leptin were higher in remitters and changes in resistin levels were negatively correlated to improvement of depressive symptoms with lithium. Our findings shed light in this pathophysiological process, which might be associated with metabolic syndrome, inflammation and other medical comorbidities in BD. |
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ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2014.02.005 |