PINAQUY, SANDRINE, HENRI CHABROL, CHANTAL SIMON, JEAN-PIERRE LOUVET, AND PIERRE BARBE. Emotional eating, alexithymia, and binge-eating disorder in obese women. Obes Res. 2003;11:195-201. Objective: To investigate the relationships between alexithymia and emotional eating in obese women with or without Binge Eating Disorder (BED). Research Methods and Procedures:One hundred sixtynine obese women completed self-report questionnaires, including the Beck Depression Inventory, the State Trait Anxiety Inventory, the Stress Perceived Scale, the Dutch Eating Behaviour Questionnaire, and the Toronto Alexithymia Scale. The presence of BED, screened using the Questionnaire of Eating and Weight Patterns, was confirmed by interview. Results: Forty obese women were identified as having BED. BED subjects and non-BED subjects were comparable in age, body mass index, educational level, and socioeconomic class. According to the Dutch Eating Behaviour Questionnaire, BED subjects exhibited higher depression, anxiety, perceived stress, alexithymia scores, and emotional and external eating scores than non-BED subjects. Emotional eating and perceived stress emerged as significant predictors of BED. The relationships between alexithymia and emotional eating in obese subjects differed between the two groups according to the presence of BED. Alexithymia was the predictor of emotional eating in BED subjects, whereas perceived stress and depression were the predictors in non-BED subjects. Discussion: This study pointed out different relationships among mood, alexithymia, and emotional eating in obese subjects with or without BED. Alexithymia was linked to emotional eating in BED. These data suggest the involvement of alexithymia in eating disorders among obese women.

1 The involvment of #I-, 12-and /3-adrenoceptors in the control of lipolysis and nutritive blood flow was investigated in abdominal subcutaneous adipose tissue of healthy young adults by use of an in situ microdialysis technique.2 Dialysis probes were infused either with isoprenaline (non-selective f,-adrenoceptor agonist), CGP 12,177 (selective #3-adrenoceptor agonist having 3,-/12-antagonist properties), dobutamine (selective 13,-adrenoceptor agonist) or terbutaline (selective 132-adrenoceptor agonist). The recovery of each probe used for perfusion was calculated by an in vivo calibration method. The local blood flow was estimated through the measurement of the escape of ethanol infused simultaneously with the drugs included in the probe. 3 Isoprenaline infusion at 0.01 gM had a weak effect while higher concentrations of isoprenaline (0.1 and 1Mm) caused a rapid, sustained and concentration-dependent increase of glycerol outflow; the maximum increase was 306+34% with 1 gM. Isoprenaline also increased the nutritive blood flow in adipose tissue; a significant effect appeared at 0.1 gM isoprenaline and was greater at 1 gM. 4 CGP 12,177 (10 and 100 Mm) increased the glycerol concentration in the dialysate (128 + 8 and 149+12%, respectively) and nutritive blood flow. Terbutaline and dobutamine (100 gM) both provoked rapid and similar increases in glycerol outflow (252 + 18 and 249 + 18%, respectively). Both, terbutaline and dobutamine increased nutritive blood flow. 5 It is concluded that 1,B-and 132-adrenoceptor subtypes are both mainly involved in the mobilization of lipids and in the control of nutritive blood flow. 133-Adrenoceptors play a weaker role in the control of lipolysis and nutritive blood flow in human subcutaneous abdominal adipose tissue.

Thyroid hormones are key regulators of metabolism that modulate transcription via nuclear receptors. Hyperthyroidism is associated with increased metabolic rate, protein breakdown, and weight loss. Although the molecular actions of thyroid hormones have been studied thoroughly, their pleiotropic effects are mediated by complex changes in expression of an unknown number of target genes. Here, we measured patterns of skeletal muscle gene expression in five healthy men treated for 14 days with 75 µg of triiodothyronine, using 24,000 cDNA element microarrays. To analyze the data, we used a new statistical method that identifies significant changes in expression and estimates the false discovery rate. The 381 up-regulated genes were involved in a wide range of cellular functions including transcriptional control, mRNA maturation, protein turnover, signal transduction, cellular trafficking, and energy metabolism. Only two genes were down-regulated. Most of the genes are novel targets of thyroid hormone. Cluster analysis of triiodothyronine-regulated gene expression among 19 different human tissues or cell lines revealed sets of coregulated genes that serve similar biologic functions. These results define molecular signatures that help to understand the physiology and pathophysiology of thyroid hormone action.

In the search for the existence of adrenergic regulation of the autocrine/paracrine function of the white adipose tissue, it was observed that conditioned media from isolated adipocytes or dialysates obtained by in situ microdialysis of human subcutaneous adipose tissue increased spreading and proliferation of 3T3F442A preadipocytes. These effects were amplified when an alpha2-adrenergic agonist was present during the obtention of conditioned media and microdialysates. This alpha2-adrenergic-dependent trophic activity was completely abolished by pretreatment of the conditioned media or microdialysates with the lysophospholipase, phospholipase B. Among the different lysophospholipids tested only lysophosphatidic acid (LPA) was able to induce spreading and proliferation of 3T3F442A preadipocytes. Moreover, previous chronic treatment of 3T3F442A preadipocytes with LPA which led to a specific desensitization of LPA responsiveness, abolished the alpha2-adrenergic-dependent trophic activities of the conditioned media and microdialysates. Finally, alpha2-adrenergic stimulation led to a rapid, sustained, and pertussis toxin-dependent release of [32P]LPA from [32P]-labeled adipocytes. Based upon these results it was proposed that in vitro and in situ stimulation of adipocyte alpha2-adrenergic receptors provokes the extracellular release of LPA leading, in turn, to regulation of preadipocyte growth.

Five adrenoceptor (AR) subtypes (beta 1, beta 2, beta 3, alpha 2 and alpha 1), are involved in the control of white and brown fat cell function. A number of metabolic events are controlled by the adrenergic system in fat cells. The stimulatory effect of catecholamines on lipolysis and metabolism is mainly connected to increments in cAMP levels, cAMP protein kinase activation and phosphorylation of various target proteins. Norepinephrine and epinephrine operate through differential recruitment of alpha 2- and beta-AR subtypes on the basis of their relative affinity for the different subtypes (the relative order of affinity is alpha 2 > beta 1 > or = beta 2 > beta 3 for norepinephrine). Antagonistic actions at the level of cAMP production exist between alpha 2- and beta 1-, beta 2- and beta 3-AR-mediated lipolytic effects in human white fat cells. The role of fat cell alpha 2-ARs, which largely outnumber beta-ARs in fat cells of certain fat deposits, in human and primate has never been clearly understood. The other AR type which is not linked to lipolysis regulation, the alpha 1-AR, is involved in the control of glycogenolysis and lactate production. Pharmacological approaches using in-situ microdialysis and selective alpha 2- and beta-AR agonists and antagonists have revealed sex- and tissue-specific differences in the adrenergic control of fat cell function and nutritive blood flow in the tissue surrounding the microdialysis probe.