Objective: To assess whether in prepubertal children insulin secretion is pulsatile as in adults and to study the influence of body weight on the pattern of insulin secretion. Design and Patients: Insulin profiles were obtained by 4-min sampling for 2 h, starting at 08.00 a.m. after an overnight fast in 10 prepubertal obese children (BMI-SDS 4.9 ± 1.6) and in 6 healthy age-matched controls. Five of the obese children were also studied after weight reduction (Δ BMI-SDS 1.6 ± 0.4). The data have been analyzed by the Pulsar program. Results: Obese children had higher mean insulin levels, insulin secretory areas under the curve above 0 (AUC₀), and AUC above baseline (AUCb), with more frequent peaks of larger amplitude and duration compared to controls. Following weight reduction there was a normalization of AUC₀ and mean insulin levels while AUCb, peak frequency, amplitude and duration did not change significantly. Correlation analysis revealed that BMI-SDS was strictly related to the parameters of pulsatile insulin secretion such as AUC₀, AUCb, mean insulin level, peak amplitude and peak frequency. Conclusions: Insulin secretion in children is pulsatile and its secretory pattern is influenced by body weight.
BackgroundObesity is a risk factor for osteoarthritis (OA). In obese subjects OA develops not only in weight-bearing joints but also in non-weight-bearing joints, suggesting that dysregulated metabolism in obese patients may promote OA onset.As obesity evolves many physiological parameters are dysregulated, including the levels of adipokine hormones such as leptin and adiponectin. For this reason, it has been suggested that adipokine levels in serum and synovial fluid are associated with a worsening of synovial inflammation and OA progression in these patients(1).In vivo and in vitro studies show that high levels of leptin induce the synthesis of metalloproteases involved in cartilage degradation(2). Conversely, dietary-induced weight loss is associated with increased adiponectin serum levels and reduced loss of tibial and femoral cartilage volume, suggesting a protective role of adiponectin in OA.STR/ort mice are an animal model of spontaneous OA characterized by early pathology development (at about 20 weeks) and dysregulated metabolism(3). Notably, these mice have adiponectin serum levels lower than those found in control mouse strains(4).ObjectivesTo evaluate whether adiponectin and leptin serum levels are associated with OA development and/or progression in STR/ort mice.MethodsFirst, we measured the time course of adipokine levels in STR/ort mice before the onset of OA (at 8, 14 and 20 weeks of age), and in age-matched CBA control mice. Then, we calculated the ratio leptin/adiponectin (L/A) in the serum of STR/ort mice during OA progression (at 20, 30 and 40 weeks). Blood samples were collected from caudal vein (time course) or from vena cava at sacrifice, when knee joints were collected, processed for histology and blindly scored according to OARSI and Mankin's methods.ResultsAdiponectin serum levels in STR/ort mice at 8, 14 and 20 weeks were significantly lower than in age-matched CBA mice. Instead, leptin serum levels in STR/ort mice were higher than in CBA strain at 14 and 20 weeks. Consequently, there was a relevant difference in the ratio L/A between the two strains, with greater L/A values in STR/ort mice at 14 and 20 weeks. (Table 1)In STR/ort mice, the ratio L/A tended to further increase between 30 and 20 weeks (1.73±0.16 from 1.28±0.17, respectively), in parallel with the increase in OARSI scores of knee joints (11.1±1.5 vs 8.4±1.3). The histopathological score increased in STR/ort mice even between 30 and 40 weeks, but without a concomitant increase in the ratio L/A.ConclusionsWe show for the first time that leptin serum levels and the ratio L/A in STR/ort mice are higher than in CBA mice, and that the ratio L/A in STR/ort mice increases as their histopathological scores worsen. We suggest that dysregulated levels of these adipokines may be associated or even precede OA development in this animal model.References
King L.K. et al. Osteoarthritis and Cartilage, 2015.Bao J.P. et all. Mol Biol Rep. 2010.Uchida K. et al. Experimental Animals, 2009.Giambelli R. et al. Osteoarthtis and Cartilage Volume 2...
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