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Objective: Increased intake of sweets or sugar craving may occur in response to chronic stress representing a risk factor for development of eating disorders and obesity. However, no safe treatment of stress‐induced sugar craving is available. In this study we analysed effects of two Lactobacillus strains on food and sucrose intake in mice before and during their exposure to a chronic mild stress (CMS). Research Methods & Procedures: C57Bl6 mice were gavaged daily for 27 days with a mix of L. salivarius (LS) LS7892 and L. gasseri (LG) LG6410 strains or with 0.9% NaCl as a control. Following 10 days of gavage, mice were individually placed into the Modular Phenotypic cages, and after 7 days of acclimation were exposed to a CMS model for 10 days. Food, water and 2% sucrose intakes as well as meal pattern were monitored. Anxiety and depressive‐like behaviour were analysed by standard tests. Results: Exposure of mice to CMS was accompanied by increased size of sucrose intake in the control group likely reflecting the stress‐induced sugar craving. A consistent, about 20% lower total sucrose intake, was observed in the Lactobacilli‐treated group during stress which was mainly due to a reduced number of intakes. Lactobacilli treatment also modified the meal pattern before and during the CMS, showing a decrease of meal number and an increase of meal size with a tendency of reduced total daily food intake. Mild anti‐depressive behavioural effects of the Lactobacilli mix were also present. Conclusion: Supplementation of mice with LS LS7892 and LG LG6410 decreases sugar consumption suggesting a potential utility of these strains against stress‐induced sugar craving. Key points: Chronic mild stress increases sugar intake in miceL. salivarius (LS) and L. gasseri (LG) probiotics mix reduces sugar intake in stressed miceLS and LG probiotics mix decreases number of meals and increases water intake in miceLS and LG probiotics mix displays mild anti‐depressive effects in stressed miceLS and LG probiotics strains mix can be useful for stress‐induced sugar craving [ABSTRACT FROM AUTHOR]

This 2023 update of the WFSBP guidelines for the pharmacological treatment of eating disorders (EDs) reflects the latest diagnostic and psychopharmacological progress and the improved WFSBP recommendations for the assessment of the level of evidence (LoE) and the grade of recommendation (GoR). The WFSBP Task Force EDs reviewed the relevant literature and provided a timely grading of the LoE and the GoR. In anorexia nervosa (AN), only a limited recommendation (LoE: A; GoR: 2) for olanzapine can be given, because the available evidence is restricted to weight gain, and its effect on psychopathology is less clear. In bulimia nervosa (BN), the current literature prompts a recommendation for fluoxetine (LoE: A; GoR: 1) or topiramate (LoE: A; GoR: 1). In binge-eating disorder (BED), lisdexamfetamine (LDX; LoE: A; GoR: 1) or topiramate (LoE: A; GoR: 1) can be recommended. There is only sparse evidence for the drug treatment of avoidant restrictive food intake disorder (ARFID), pica, and rumination disorder (RD). In BN, fluoxetine, and topiramate, and in BED, LDX and topiramate can be recommended. Despite the published evidence, olanzapine and topiramate have not received marketing authorisation for use in EDs from any medicine regulatory agency. [ABSTRACT FROM AUTHOR]

Introduction: Neurotensin (NTS) is a 13-amino acid neuropeptide functionally linked with the brain dopaminergic system via expression of the NTS peptide or its receptor in dopamine neurons. Neuropeptide-binding immunoglobulins (Igs) are present in humans and can be involved in both physiological and pathological processes. Considering the functional link between NTS and dopamine neurons, we studied the occurrence of NTS-binding IgG autoantibodies in patients with Parkinson's disease (PD). Methods: Plasma levels of NTS-binding IgG were analyzed using enzyme-linked immunosorbent assay in both male and female PD patents and in age-matched healthy controls. Possible microbial origin of NTS cross-reactive IgG was analyzed by sequence alignment of the 6-amino acid C-terminal NTS pharmacophore with bacterial and viral proteins from the public NCBI database. Results: NTS-binding IgG were detected in the plasma of all study subjects, while their levels were consistently lower in PD patients versus controls (p = 0.0001), independently from age or sex of the study participants. Moreover, PD patients with a more severe stage (2.5–3.0) of the disease had lower levels of NTS-binding IgG (p = 0.0004) than those with a milder stage (1.0–2.0). Furthermore, PD patients taking amantadine or high doses of levodopa had higher levels of NTS-binding IgG than those without medication. Contiguous sequence homology for the NTS pharmacophore was present in several microbial proteins occurring in human gut microbiota. Discussion: The study revealed that NTS-binding IgG occur naturally in humans and that PD patients display their low plasma levels accentuated by disease severity. The functional significance of this finding and its relevance to the pathophysiology of PD, including putative link to gut microbiota, remain to be studied. [ABSTRACT FROM AUTHOR]

The hypothalamic arcuate nucleus is involved in the control of energy intake and expenditure and may participate in the pathogenesis of eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). Two systems are of particular interest in this respect, synthesizing [alpha]-melanocyte-stimulating hormone ([alpha]-MSH) and synthesizing neuropeptide Y, respectively. We report here that 42 of 57 (74%) AN and/or BN patients studied had in their plasma Abs that bind to melanotropes and/or corticotropes in the rat pituitary. Among these sera, 8 were found to bind selectively to [alpha]-MSH-positive neurons and their hypothalamic and extrahypothalamic projections as revealed with immunostaining on rat brain sections. Adsorption of these sera with [alpha]-MSH peptide abolished this immunostaining. In the pituitary, the immunostaining was blocked by adsorption with [alpha]-MSH or adrenocorticotropic hormone. Additionally, 3 AN/BN sera bound to luteinizing hormone-releasing hormone (LHRH)-positive terminals in the rat median eminence, but only 2 of them were adsorbed with LHRH. In the control subjects, 2 of 13 sera (16%) displayed similar to AN/BN staining. These data provide evidence that a significant subpopulation of AN/BN patients have autoantibodies that bind to [alpha]-MSH or adrenocorticotropic hormone, a finding pointing also to involvement of the stress axis. It remains to be established whether these Abs interfere with normal signal transduction in the brain melanocortin circuitry/LHRH system and/or in other central and peripheral sites relevant to food intake regulation, to what extent such effects are related to and/or could be involved in the pathophysiology or clinical presentation of AN/BN, and to what extent increased stress is an important factor for production of these autoantibodies.

As revealed by previous microdialysis studies, basal and food intake-accompanied dopamine re]ease significantly differs in the hypothalamus of obese vs. lean Zucker rats. In the present study, we determined whether dopaminergic receptors are also compromised in obesity. Dopaminergic [D.sub.1] and [D.sub.2] receptor mRNA expression was studied in the ventromedial hypothalamus (VMH), lateral hypothalamic area (LHA), and the adenohypophysis (AH) of obese and lean Zucker rats using RT-PCR technique. In obese Zucker rats, we found an upregulation of [D.sub.1] receptor mRNA in the VMH and AH and a downregulation in the LHA, whereas [D.sub.2] receptor mRNA was downregulated in both the VMH and LHA, but not changed in the AH, compared with lean rats. Also, an increase of [D.sub.1] receptor staining was seen in the paraventriculerc nucleus of obese rats by immunohistochemistry. We selected the VMH to test if the observed changes in the dopamine receptor expression of obese rats induce behavioral sensitization to dopamine as expressed by hyperphagia. The overnight food-deprived rats received a single VMH injection (10 nmol) of sulpiride ([D.sub.2] receptor antagonist) or saline as control, then food was provided and 1-h food intake was measured. Food intake after sulpiride vs. saline injection was greater in obese rats but was not different in lean rats. Our data suggest that downregulation of [D.sub.2] receptor in the hypothalamus at least in the VMH induces behavior sensitization for having large meals. Low [D.sub.2] receptor expression may be causal for an exaggerated dopamine release observed in obese rats during food ingestion and for reduced satiety feedback effect of dopamine. High level of [D.sub.1] receptor expression in the VMH and low in the LHA may also contribute to the specific feeding pattern in obese rats represented by large meal size and low meal number. monoamine; meal size

Sato, Tomoi, Michael M. Meguid, Serguei O. Fetissov, Chung Chen, and Lihua Zhang. Hypothalamic dopaminergic receptor expressions in anorexia of tumor-bearing rats. Am J Physiol Regulatory Integrative Comp Physiol 281: R1907-R1916, 2001.--Our past microdialysis studies in ventromedial hypothalamic nucleus (VMN) and lateral hypothalamic area (LHA) of changes in dopamine concentrations in response to changes in food intake [characterized as feeding pattern (changes in meal number and size)] in anorexia of cancer show abnormal presynaptic dopaminergic neurotransmission. To determine postsynaptic receptor status, studies were done in tumor-bearing (TB) and non-tumor-bearing (NTB) free-feeding control rats while continuously measuring their food intake via a rat eater meter. When TB rats developed anorexia, TB and control rats were killed, and postsynaptic [D.sub.1]- and [D.sub.2]-receptor mRNA expression in LHA and VMN were measured via RT-PCR. At anorexia, food intake decreased initially by a decrease in meal number, whereas a concurrent increase in meal size occurred for 24 h in an attempt to maintain food intake constant. Then meal size also decreased. At this time, [D.sub.1]-and [D.sub.2]-receptor mRNA expressions in LHA and VMN of TB vs. controls were significantly upregulated. Verification of [D.sub.1]- or [D.sub.2]-receptor changes to changes in meal number and size at anorexia was made by injection of intra-VMN or -LHA dopaminergic receptor antagonists. Intra-VMN [D.sub.1]-receptor antagonist (SCH-23390) in TB rats decreased food intake mainly via a decrease in meal size. Intra-VMN [D.sub.2]-receptor antagonist (sulpiride) in TB rats increased food intake via an increase in meal number and in NTB free-feeding rats by an increase in meal size. Intra-LHA [D.sub.1]-receptor antagonist in TB rats had no effect on food intake or feeding pattern. Intra-LHA [D.sub.2]-receptor antagonist in TB and in NTB free-feeding rats increased food intake via an increase in meal number. Our data provide evidence that postsynaptic dopaminergic receptor subtypes in the hypothalamus are involved in the regulation of meal size, meal number, and thus food intake in anorectic TB rats. messenger RNA; dopaminergic receptor antagonist; sulpiride; SCH-23390; meal size; meal number Received 21 August 2000; accepted in final form 22 August 2001