Oxidation of High Doses of Serotonin Favors Lipid Accumulation in Mouse and Human Fat Cells.

Oxidation of high doses of serotonin favors lipid accumulation in mouse and human fat cells.

Filed under: Eating Disorders

Mol Nutr Food Res. 2013 Feb 6;
Grès S, Canteiro S, Mercader J, Carpéné C

SCOPE: The ingestion of serotonin-rich food (bananas, chocolate) increases 5-hydroxytryptamine (5-HT) in blood and its corresponding oxidation products in urines but without direct central consequences since the neurotransmitter does not easily cross the blood-brain barrier. However, there are numerous peripheral effects of serotonin, and recently, 5-HT aldehydic oxidation products have been demonstrated to behave as ligands of peroxisome proliferator-activated receptor ? (PPAR-?). Since this nuclear factor manages lipid handling by adipose tissue, the response of fat cells to 5-HT exposure needed further investigation. METHODS AND RESULTS: Serotonin oxidation was studied on human adipose tissue homogenates and mouse 3T3F442A preadipocytes by fluorometric and radiometric methods. Gene expression was assessed by real-time RT-PCR in human adipocytes and in 3T3F442A after mid- and long-term exposure to 5-HT while triacylglycerols and proteins were assessed by spectrophotometry. Six-hour exposure of human adipocytes to 250 ?M 5-HT increased gene expression of lipid-binding proteins, glucose carriers, and enzymes of triacylglycerol synthesis (FABP4, CD36, GLUT1, and phosphoenolpyruvate carboxykinase), as did rosiglitazone treatment. Long-term serotoninergic stimulation of cultured 3T3F442A preadipocytes by 100-250 ?M 5-HT enhanced fat storage and upregulation of PPAR-?-responsive genes, in a manner sensitive to MAO- or PPAR-? inhibition. Our observations suggest an unpredicted peripheral effect of serotonin on adipose tissue that depends on its amine oxidation. CONCLUSION: Besides being centrally active on eating behavior, 5-HT may promote PPAR-? activation and subsequent lipogenic effects in fat cells, raising the interest to consider its level in future diet formulations.
HubMed – eating

Intestinal Absorption and Pancreatic Function are Preserved in Anorexia Nervosa Patients in Both a Severely Malnourished State and After Recovery.

Filed under: Eating Disorders

Eur Eat Disord Rev. 2013 Feb 7;
Martínez-Olmos MA, Peinó R, Prieto-Tenreiro A, Lage M, Nieto L, Lord T, Molina-Pérez E, Domínguez-Muñoz JE, Casanueva FF

INTRODUCTION: Anorexia nervosa (AN) is characterised by a refusal to normal body weight accompanied by a marked restriction of food intake, frequently leading to severe malnutrition. In severe malnutrition and wasting syndromes, mucosal atrophy, altered gastrointestinal motility and pancreatic atrophy, which alter digestive function and can exacerbate malnutrition, have been described. The objective of this work was to determine intestinal absorption and pancreatic function in severely malnourished AN patients before and after recovery. METHODS: Ten severely malnourished AN women were studied at hospital admittance (body mass index?=?11.44-16.16?kg/m(2) ) and after weight recovery with artificial nutrition (body mass index???20?kg/m(2) ). A (13) C-labelled triglycerides digestion test, faecal elastase test and d-xylose absorption test were performed. RESULTS: In nine patients, (13) C-labelled triglycerides digestion tests and the faecal elastase and d-xylose tests were normal both before and after weight recovery. In one patient, the results were abnormal, and they led to the detection of a previously undiagnosed celiac disease in addition to her AN. CONCLUSION: In this series, there was neither intestinal absorption nor pancreatic function disturbances in severely malnourished AN patients either before or after weight recovery. The usefulness of these tests in the differentiation of functional versus structural changes needs further studies. Copyright © 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
HubMed – eating

Eating Epilepsy is Associated With Initial Precipitating Events and Therapy Resistance.

Filed under: Eating Disorders

Clin EEG Neurosci. 2013 Feb 6;
Kokes U, Baykan B, Bebek N, Gurses C, Gokyigit A

We present the characteristics of eating epilepsy (EE), which is an underrecognized and complex form of reflex epilepsy. The files of 8996 patients with epilepsy were investigated retrospectively and only 6 cases (0.067%) were found.  Four males and 2 females, aged 20 to 63 years, had focal seizures, mostly with dyscognitive and experiential aura triggered by eating, as well as spontaneous seizures. All had an initial precipitating event for seizures (such as head/birth trauma or encephalitis). In 4 patients, the seizures were induced in the middle of the meal or even closely after the end. In the remaining 2 cases the seizures were at the beginning of the meal, suggesting 2 different mechanisms. Two patients had normal magnetic resonance imaging (MRI), whereas the others had heterogeneous findings. The interictal electroencephalographs (EEGs) showed frequent spikes over a large area on the left temporal region in 5 and over the right temporal area in 1 case. We recorded eating-related seizures originating from the left temporal region in 3 cases. Positron-emission tomography (PET) investigations were concordant with the EEG foci in 2 patients. All but 1 had a therapy-resistant course. Our study suggested that EE is extremely rare and occurred many years after an initial precipitating event for seizures. These focal seizures, starting mostly with experiential/dyscognitive aura, usually originated from the left temporal region, had mostly a therapy-resistant course, and were triggered by different mechanisms during eating with a long latency in most of the cases.
HubMed – eating

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