Ligands and receptors of the TNF superfamily are decreased in major depression and during early antidepressant therapy.

BACKGROUND: The up-regulation of pro-inflammatory agents, amongst them tumor necrosis factor (TNF), may represent low-grade inflammation in major depression. To further elucidate inflammatory mechanisms related to TNF in depression, the aim of the current study was to investigate the involvement of ligands and receptors of the TNF/TNF-receptor-superfamily yet un- or little explored in major depression. METHODS: Serum levels of ligands (TNF, TNF-related weak inducer of apoptosis [TWEAK], B-cell activating factor [BAFF], tumor necrosis factor superfamily member 14 [TNFSF14; LIGHT], A proliferation-inducing ligand [APRIL]) and receptor molecules (TNF receptor superfamily member 8 [TNFRSF8; sCD30], soluble TNF receptor type 1 [sTNFR1] and type 2 [sTNFR2]) of the TNF/TNF-receptor-superfamily were measured in 50 unmedicated patients suffering from major depression and 48 healthy controls and were reassessed in 37 of the depressed patients two weeks after the initiation of antidepressive treatment. RESULTS: In comparison to the healthy controls, the interrelated serum levels of TWEAK, BAFF, TNFSF8, sTNFR1 and sTNFR2 were reduced both in the unmedicated and medicated depressed patients. Serum levels of BAFF and TNF significantly increased during the initiation of antidepressive treatment. In the combined sample of unmedicated depressed and healthy controls, but not the separate groups, scores of the BDI-II inversely correlated with levels of TWEAK, BAFF, sTNFR1, sTNFR2 and TNFSF8. CONCLUSION: The current findings give evidence for a role of the TNF/TNF-receptor-superfamily in the pathophysiology of major depression that may involve reduced tissue regeneration and neurogenesis rather than an acceleration of pro-inflammatory pathways.

A preliminary study on the variability of blood glucose following meal consumption as it relates to differences in oral glucose tolerance in young adults.

Insulin resistance (IR) affects the ability to maintain normal glycemia and places one at greater risk of the development of disease. The aim of this study was to assess IR via the administration of an oral glucose tolerance test (OGTT) and then determine the relationship between IR and postprandial blood glucose levels in young adults 19-24 years of age. Following a 10 hour fast, 10 men and 10 women completed an OGTT and in three subsequent weeks consumed high, medium, and low glycemic load (GL) meals in random order. Fasted and two-hour (2 h) blood glucose levels were determined. Height, weight, and waist circumference were measured and subjects completed a questionnaire recording recent weight gain, family history of diabetes, and physical fitness. Although all fasted blood glucose levels were normal, two subjects classified as impaired glucose tolerant based on 2 h OGTT values >140 mg/dL. OGTT and high glycemic load meal 2 h blood glucose levels were highly significantly correlated (p = 0.0012). Significantly higher blood glucose levels were also found in women, high BMI, low fitness, and rapid weight gain groups. Although limited by a small sample, these preliminary data suggest that glycemic response to meal ingestion is based on both the GL of the meal and the individual's level of IR.