Inflammation Markers in Type 2 Diabetes and the Metabolic Syndrome in the Pediatric Population.

PURPOSE OF REVIEW: Chronic inflammation, adipokines, and hepatokines have been identified as basis of insulin resistance and ß cell failure in animal models. We present our current knowledge concerning the potential relationship between these cytokines, inflammation, metabolic syndrome (MetS), and type 2 diabetes mellitus (T2DM) in the pediatric population. RECENT FINDINGS: Pro-inflammatory cytokines related to insulin resistance and MetS in children are tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1ß, interferon gamma, pigment epithelium-derived factor, chemerin, vaspin, and fetuin A. Anti-inflammatory cytokines associated with insulin resistance and MetS in children are leptin, adiponectin, omentin, fibroblast growth factor (FGF)-21, osteocalcin, and irisin. These anti-inflammatory cytokines are decreased (adiponectin, omentin, and osteocalcin) or increased (leptin, FGF-21, and irisin) in obesity suggesting a resistance state. TNF-α, fetuin A, and FGF-21 are altered in obese children with T2DM suggesting an involvement in ß cell failure. These cytokines, adipokines, and hepatokines may be able to predict development of MetS and T2DM and have a potential therapeutic target ameliorating insulin resistance.

Effects of methylphenidate on weight gain and food intake in hypothalamic obesity.

UNLABELLED: For patients with a craniopharyngioma (CP), treatment of hypothalamic obesity (HO) and hyperphagia following resection and/or radiotherapy is extremely difficult and few reports have been published on potential drug therapies. Psychomotor stimulant methylphenidate (MPH) has been reported to inhibit food intake (FI). In this paper, we report reduction of body mass index (BMI) and appetite in an adolescent CP patient suffering from HO. We then tested the ability of MPH to attenuate the FI and body weight (BW) gain in a rat model consistent with the neuroanatomical and metabolic disturbances commonly observed in obese CP patients. Specifically, we used a novel electrolytically generated combined medial hypothalamic lesion (CMHL) affecting the arcuate nucleus, ventromedial hypothalamic nucleus, and dorsomedial hypothalamic nucleus to induce hyperphagia, rapid weight gain, and adiposity. Both CMHL and control animals (n = 7 per group) were administered either methylphenidate HCl (MPH; 20 mg kg(-1) day(-1)) or saline for 4 days in a crossover design experiment 28 weeks post-surgery. A significant decrease in percent baseline FI (CMHL -23%, p = 0.008; control -20%, p = 0.002) and percent change in BW (CMHL -1.97%/4 days, p = 0.011; control -1.75%/4 days, p = 0.003) was observed during MPH treatment as compared to saline. CONCLUSION: This study shows MPH treatment of severely obese CMHL rats resulted in significantly reduced FI and BW loss.