Relationship between sleep duration and childhood obesity: Systematic review including the potential underlying mechanisms.

AIM: The prevalence of obesity is continually increasing worldwide. Determining risk factors for obesity may facilitate effective preventive programs. The present review focuses on sleep duration as a potential risk factor for childhood obesity. The aim is to summarize the evidence on the association of sleep duration and obesity and to discuss the underlying potential physiological and/or pathophysiological mechanisms. DATA SYNTHESIS: The Ovid MEDLINE, Scopus and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched for papers using text words with appropriate truncation and relevant indexing terms. All studies objectively measuring sleep duration and investigating the association between sleep duration and obesity or factors (lifestyle and hormonal) possibly associated with obesity were included, without making restrictions based on study design or language. Data from eligible studies were extracted in tabular form and summarized narratively. After removing duplicates, 3540 articles were obtained. Finally, 33 studies (including 3 randomized controlled trials and 30 observational studies) were included in the review. CONCLUSION: Sleep duration seems to influence weight gain in children, however, the underlying explanatory mechanisms are still uncertain. In our review only the link between short sleep duration and the development of insulin resistance, sedentarism and unhealthy dietary patterns could be verified, while the role of other mediators, such as physical activity, screen time, change in ghrelin and leptin levels, remained uncertain. There are numerous evidence gaps. To answer the remaining questions, there is a need for studies meeting high methodological standards and including a large number of children.

Characterization of long-term gait deficits in mouse dMCAO, using the CatWalk system.

Evaluation of functional outcome is widely used across species to assess the recovery process following various pathological conditions, including spinal cord injury, musculo-skeletal injury, mithochondrial disease, neuropathic cancer, Huntington's disease, chronic pain, cortical lesion, and olivocerebellar degeneration among others. The Stroke Therapy Academic Industry Roundtable (STAIR) recommends multiple endpoints for behavioral studies in pre-clinical stroke research, to demonstrate their clinical relevance. One of the more challenging tasks in experimental stroke research is measuring long-term functional outcome in mice. It is, however, becoming more important, since transgenic mice are increasingly used for modeling human neurological disorders. Using CatWalk, we characterized long-lasting gait/locomotion deficits following mouse distal middle cerebral artery occlusion (dMCAO). The post-dMCAO assessment was performed at 7, 14, 21, and 28days after experimental ischemia. When compared to sham-operated mice, dMCAO animals displayed a statistically significant decrease in Spatial parameters (such as Paw Area), while the Temporal parameters (Stand, Initial and Terminal Dual Stances) were significantly increased for three weeks after surgery. Kinetic parameters were significantly decreased in dMCAO animals at 7days after dMCAO. The Interlimb coordination group of parameters displayed the strongest deficits at 21days. While CatWalk variables were altered in all paws, the degree of change was greatest for the parameters measured from the Right Front Paw (contralateral to the lesion). All parameters measured in dMCAO and Sham-operated groups reached similar levels at four weeks after the experimental insult, which reflects a spontaneous post-ischemic recovery. Based on our investigation, we conclude that CatWalk represents a relevant and sensitive analysis, which allows long-term characterization of animal functional recovery in the dMCAO model of experimental ischemia.

Nasal vaccination of young rainbow trout (Oncorhynchus mykiss) against infectious hematopoietic necrosis and enteric red mouth disease.

Determining the earliest age at which farmed fish can be successfully vaccinated is a very important question for fish farmers. Nasal vaccines are novel mucosal vaccines that prevent aquatic infectious diseases of finfish. The present study investigates the ontogeny of the olfactory organ of rainbow trout by histology and aims to establish the earliest age for vaccination against infectious hematopoietic necrosis (IHN) and enteric red mouth (ERM) disease using the nasal route. Rainbow trout (Oncorhynchus mykiss) were vaccinated intranasally (I.N) at three different ages: 1050° days (DD) (group A); 450 DD (group B); and 360 DD (group C), or 70, 30 and 24 days post-hatch (dph), respectively. The mean weights of groups A, B and C were 4.69 g, 2.9 g and 2.37 g, respectively. Fish received either a live attenuated IHN virus vaccine, ERM formalin killed bacterin or saline (mock vaccinated). Fish were challenged to the corresponding live pathogen 28 days post-vaccination. IHN vaccine delivery at 360 DD resulted in 40% mortality likely due to residual virulence of the vaccine. No mortality was observed in the ERM nasal delivery groups. Following challenge, very high protection rates against IHN virus were recorded in all three age groups with survivals of 95%, 100% and 97.5% in groups A, B and C, respectively. Survival against ERM was 82.5%, 87.5% and 77.5% in groups A, B and C, respectively. Survival rates did not differ among ages for either vaccine. Our results indicate the feasibility and effectiveness of nasal vaccination as early as 360 DD and vaccination-related mortalities when a live attenuated viral vaccine was used in the youngest fish.

Plasma levels of acylated ghrelin during an oral glucose tolerance test in obese children.

OBJECTIVE: Ghrelin is an acylated peptide with octanoyl modification, which is essential for its GH-releasing ability. Coexpression of GH secretagogue receptor (GHS-R) and ghrelin in the pancreas suggests that this peptide is involved in glucose metabolism. The other form of the molecule, the non-acylated ghrelin, has been reported to be devoid of any pituitaric endocrine activities. Previous reports demonstrated that plasma total ghrelin levels decrease after oral glucose administration in obese children, but no data are available about the plasma levels of acylated ghrelin. Therefore, in the present study the plasma levels of acylated ghrelin were measured in obese and control children during oral glucose tolerance test (OGTT). MATERIALS AND METHODS: Acylated ghrelin response to OGTT was evaluated in 11 obese and 9 age-matched control children. All subjects received 0.75 g/kg (maximum 75 g) glucose solution orally after an overnight fast. Acylated ghrelin, insulin, glucose, and GH were determined at 0, 30, 60 and 120 min, and leptin at 0 min of the OGTT. RESULTS: Plasma basal levels of acylated ghrelin were significantly lower in the obese children than in the controls (66.3+/-6.7 vs 97.2+/-14.4 pg/ml, p<0.05). The plasma acylated ghrelin concentration decreased significantly at 30 and 60 min in the control group (53.3+/-9.9 and 57.4+/-7.0 pg/ml, p<0.05), but not in the obese group (64.7+/-9.6 and 49.3+/-4.6 pg/ml) as compared to the basal value. In the obese group the acylated ghrelin level was significantly higher at 120 min, than at 0 min (91.6+/-9.8 vs 66.3+/-6.7 pg/ml, p<0.05). CONCLUSIONS: There was no rapid fall in plasma levels of acylated ghrelin in obese children after OGTT at 30 min, but there was an increase at 120 min, suggesting that the dynamic of the response to OGTT is slower and there is an upregulation of active ghrelin in the second half of OGTT in obese children.

Behavioral changes induced by cocaine in mice are modified by a hyperlipidic diet or recombinant leptin

The objective of the present study was to determine if the acute behavioral effects of cocaine acutely administered intraperitoneally (ip) at doses of 5, 10 and 20 mg/kg on white male CF1 mice, 90 days of age, would be influenced by leptin acutely administered ip (at doses of 5, 10 and 20 æg/kg) or by endogenous leptin production enhanced by a high-fat diet. The acute behavioral effects of cocaine were evaluated in open-field, elevated plus-maze and forced swimming tests. Results were compared between a group of 80 mice consuming a balanced diet and a high-fat diet, and a group of 80 mice fed a commercially available rodent chow formula (Ralston Purina) but receiving recombinant leptin (rLeptin) or saline ip. Both the high-fat-fed and rLeptin-treated mice showed decreased locomotion in the open-field test, spent more time in the open arms of the elevated plus-maze and showed less immobility time in the forced swimming test (F(1,68) = 7.834, P = 0.007). There was an interaction between diets and cocaine/saline treatments in locomotion (F(3,34) = 3.751, P = 0.020) and exploration (F(3,34) = 3.581, P = 0.024). These results suggest that anxiolytic effects and increased general activity were induced by leptin in cocaine-treated mice and that low leptin levels are associated with behavioral depression. Chronic changes in diet composition producing high leptin levels or rLeptin treatment may result in an altered response to cocaine in ethologic tests that measure degrees of anxiety and depression, which could be attributed to an antagonistic effect of leptin.

Two cases of musculoskeletal syndrome associated with acne.

We report two cases of musculoskeletal syndrome (myalgia, arthralgia, arthritis, hyperostosis) that developed in male adolescents who had severe acne (acne conglobata and acne fulminans). In both patients the hyperostosis of the right clavicle aroused the suspicion of a bone tumor or osteomyelitis, which was excluded by histologic examination. Radiologic and laboratory characteristics of musculoskeletal syndrome associated with acne conglobata and acne fulminans are reviewed as well as isotretinoin therapy. The problems of differential diagnosis are also discussed.