Neurocentre Magendie

Daniela COTA


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Médecine, Univ. Bologne, Italie (1999)
Postdoc Institut Max-Planck, Munich (20012003)
Postdoc Univ. Cincinnati, USA (2004-2007)
CR1 à l'Inserm (2008)

Oct 1999: Degree in Medicine and Surgery (M.D., Magna cum Laude), University of Bologna, Italy
May 2000: Medical license

Since January 2008: CR1 INSERM and Avenir Group Leader, Avenir Group: “Régulation de l'équilibre énergétique et obésité” (physiopathology of energy balance and obesity), NeuroCentre Magendie, Bordeaux, France
2004– 2007: Postdoctoral Fellow with Profs. R. J. Seeley and S. C. Woods, Obesity Research Center, University of Cincinnati, USA
2001–2003: Postdoctoral Fellow with Profs. G. K. Stalla and U. Pagotto, Clinical Neuroendocrinology Group, Max-Planck institute of Psychiatry, Munich, Germany
2001–2003: Medical School of Specialization in Endocrinology and Metabolic Disorders, Director Prof. Renato Pasquali, University of Bologna, Italy


56 publication(s) depuis Juin 2000:

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* equal contribution
Les IF indiqués ont été collectés par le Web of Sciences en

10/2003 | J Endocrinol Invest   IF 2.6
Antagonizing the cannabinoid receptor type 1: a dual way to fight obesity.
Cota D, Genghini S, Pasquali R, Pagotto U


08/2003 | J Clin Invest   IF 12.8
The endogenous cannabinoid system affects energy balance via central orexigenic drive and peripheral lipogenesis.
Cota D, Marsicano G, Tschop M, Grubler Y, Flachskamm C, Schubert M, Auer D, Yassouridis A, Thone-Reineke C, Ortmann S, Tomassoni F, Cervino C, Nisoli E, Linthorst AC, Pasquali R, Lutz B, Stalla GK, Pagotto U

The cannabinoid receptor type 1 (CB1) and its endogenous ligands, the endocannabinoids, are involved in the regulation of food intake. Here we show that the lack of CB1 in mice with a disrupted CB1 gene causes hypophagia and leanness. As compared with WT (CB1+/+) littermates, mice lacking CB1 (CB1-/-) exhibited reduced spontaneous caloric intake and, as a consequence of reduced total fat mass, decreased body weight. In young CB1-/- mice, the lean phenotype is predominantly caused by decreased caloric intake, whereas in adult CB1-/- mice, metabolic factors appear to contribute to the lean phenotype. No significant differences between genotypes were detected regarding locomotor activity, body temperature, or energy expenditure. Hypothalamic CB1 mRNA was found to be coexpressed with neuropeptides known to modulate food intake, such as corticotropin-releasing hormone (CRH), cocaine-amphetamine-regulated transcript (CART), melanin-concentrating hormone (MCH), and preproorexin, indicating a possible role for endocannabinoid receptors within central networks governing appetite. CB1-/- mice showed significantly increased CRH mRNA levels in the paraventricular nucleus and reduced CART mRNA levels in the dorsomedial and lateral hypothalamic areas. CB1 was also detected in epidydimal mouse adipocytes, and CB1-specific activation enhanced lipogenesis in primary adipocyte cultures. Our results indicate that the cannabinoid system is an essential endogenous regulator of energy homeostasis via central orexigenic as well as peripheral lipogenic mechanisms and might therefore represent a promising target to treat diseases characterized by impaired energy balance.

03/2003 | Int J Obes Relat Metab Disord
Endogenous cannabinoid system as a modulator of food intake.
Cota D, Marsicano G, Lutz B, Vicennati V, Stalla GK, Pasquali R, Pagotto U

The ability of Cannabis sativa (marijuana) to increase hunger has been noticed for centuries, although intensive research on its molecular mode of action started only after the characterization of its main psychoactive component Delta(9)-tetrahydrocannabinol in the late 1960s. Despite the public concern related to the abuse of marijuana and its derivatives, scientific studies have pointed to the therapeutic potentials of cannabinoid compounds and have highlighted their ability to stimulate appetite, especially for sweet and palatable food. Later, the discovery of specific receptors and their endogenous ligands (endocannabinoids) suggested the existence of an endogenous cannabinoid system, providing a physiological basis for biological effects induced by marijuana and other cannabinoids. Epidemiological reports describing the appetite-stimulating properties of cannabinoids and the recent insights into the molecular mechanisms underlying cannabinoid action have proposed a central role of the cannabinoid system in obesity. The aim of this review is to provide an extensive overview on the role of this neuromodulatory system in feeding behavior by summarizing the most relevant data obtained from human and animal studies and by elucidating the interactions of the cannabinoid system with the most important neuronal networks and metabolic pathways involved in the control of food intake. Finally, a critical evaluation of future potential therapeutical applications of cannabinoid antagonists in the therapy of obesity and eating disorders will be discussed.

12/2001 | Eat Weight Disord-st   IF 1.8
Relationship between socio-economic and cultural status, psychological factors and body fat distribution in middle-aged women living in Northern Italy.
Cota D, Vicennati V, Ceroni L, Morselli-Labate AM, Pasquali R.


11/2000 | Recenti Prog Med
[Steroid therapy and adrenal function].
Cota D, Ceroni L, Pasquali R

Glucocorticoids are frequently used for both diagnostic and therapeutic purposes. Their action mimics endogenous glucocorticoid actions by altering the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Therefore, they can be responsible for iatrogenic diseases, particularly if used at high doses and for a long time. The aim of this brief review is to show the main pharmacological characteristics and the endocrine effects of glucocorticoids. The HPA axis insufficiency, related to acute glucocorticoid withdrawal, is also discussed.

06/2000 | Minerva Endocrinol   IF 1.4
[Pseudo-Cushing syndrome. Physiopathologic aspects and differential diagnosis].
Ceroni L, Cota D, Pasquali R

Pseudo-Cushing Syndromes (PCS) are a heterogeneous group of disorders, including alcoholism and depression, that share many of the clinical and biochemical features of Cushing's Syndrome (CS). It has been suggested that hypercortisolism of PCS may be the result of increased hypothalamic corticotropin-releasing hormone secretion in the context of a hypothalamic-pituitary-adrenal axis that is otherwise normally constituted. The substantial overlap in clinical features and daily urinary free cortisol levels between several patients with CS and those with PCS can make the differential diagnosis difficult. The most accurate tests in the distinction of CS from alcohol-induced PCS are dexamethasone-CRH and a midnight serum cortisol measurement. In depressed patients, the insulin tolerance test may be useful, although some overlap may exist. This brief review summarises the principal pathophysiological events of PCS and provides a useful strategy for differential diagnosis.