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Background: Accurately determining energy requirements is key for nutritional management of pediatric obesity. Recently, a portable handheld indirect calorimeter, MedGem (MG) has become available to measure resting energy expenditure (REE). Our work aims to determine the clinical validity and usefulness of MG to measure REE in overweight and obese adolescents., Methods: Thirty-nine overweight and obese adolescents (16 male (M): 23 female (F), 15.2 ± 1.9 y, BMI percentile: 98.6 ± 2.2%) and 15 normal weight adolescents (7M: 8F, age 15.2 ± 2.0 y, BMI percentile: 39.2 ± 20.9%) participated. REE was measured with both MG and standard indirect calorimeter (VMax) in random order., Results: MG REE (1,600 ± 372 kcal/d) was lower than VMax REE (1,727 ± 327 kcal/) in the overweight and obese adolescents. Bland Altman analysis (MG -VMax) showed a mean bias of -127 kcal/d (95% CI = -72 to -182 kcal/d, P < 0.001), and a proportional bias existed such that lower measured REE by VMax was underestimated by MG, and higher measured REE by VMax were overestimated by MG., Conclusion: MG systematically underestimates REE in the overweight and adolescent population, thus the MG portable indirect calorimeter is not recommended for routine use. Considering that it is a systematic underestimation of REE, MG may be clinically acceptable, only if used with caution.

Maintenance of normal glucose homeostasis is crucial for survival during the perinatal period. Acylated ghrelin (AG) but not unacylated ghrelin (UAG) inhibits insulin release from pancreatic islets in adult rats. Circulating AG concentrations are low in the fetus and progressively increase in the postnatal period. We tested the hypothesis that AG has insulinostatic effects in vitro and in vivo during the perinatal period. In vitro, AG (10(-10)-10(-8) M) caused a 25-53% decrease in insulin secretion by islets from 5-d-old rat pups under normo- and hyperglycemic conditions, an effect that was mediated through the growth hormone secretagogue receptor (GHSR- 1a). Ghrelin (1-5) amide, [Dap3]-octanoyl, a pentapeptide that is resistant to deacylation and binds the GHSR-1a, had similar effects at 10(-8) M. In vivo, AG, UAG, or GHRP-6 [D-Lys3], a GHSR-1a antagonist, did not affect insulin or glucagon concentrations during the first 3 h of life. In 6-d-old pups, AG, UAG, or ghrelin (1-5) amide, [Dap3]-octanoyl did not affect glucose-induced insulin or C-peptide concentrations. In summary, AG has insulinostatic effects in vitro as early as during the perinatal period. These effects could not be confirmed in vivo, possibly due to the short half-life of AG in rat neonates.

The processing of preproghrelin in the stomach by prohormone convertase (PC) 1/3 produces ghrelin and possibly obestatin. In the neonate, the pancreas is also a major source of ghrelin. We compared the ontogeny of preproghrelin, ghrelin, obestatin, and PCs in the stomach and pancreas from rat embryos (day 21) and neonates (days 1, 6, 13, 21, and 28) by immunohistochemistry. In stomach, preproghrelin positive cells were present from embryonic day 21 and were in excess of ghrelin cells. The number of ghrelin positive cells progressively increased with age. When preproghrelin cells were immunoreactive for ghrelin, they were also immunoreactive for obestatin and PC1/3. In pancreas, we only found 0 to 2 preproghrelin positive cells per islet and each of these cells was also positive for ghrelin and obestatin. None of the ghrelin positive cells stained for insulin, but we observed ghrelin positive/glucagon negative and ghrelin positive/glucagon positive cells. Ghrelin positive cells contained PC1/3 or PC2. In summary, in stomach, an excess of preproghrelin positive cells compared with ghrelin/PC1/3 positive cells suggests that PC1/3 determines preproghrelin processing to ghrelin. In pancreas, the colocalization of PC1/3 or PC2 in ghrelin positive cells points to a role for both PCs in preproghrelin processing.

The leptin to fat ratio early in life could contribute to fixing the set point of leptin feedback at the hypothalamic level. Subjects from Asian and Caucasian ethnicities differ in body composition. We tested the hypothesis that anthropometric markers and their relationship to umbilical cord leptin, cortisol and cortisone, DHEAs and oestriol differed between Caucasians and Asians at birth. Birthweight, length, arm, calf and abdominal circumferences, scapular, triceps, quadriceps and abdominal skinfolds were measured in 180 healthy, full-term newborns of Asian and Caucasian ethnicities. Leptin and steroid hormone concentrations were determined in umbilical cord plasma. There was a significant difference in the slope of the regression between leptin and birthweight (p = 0.03) and calf circumference (p = 0.05) between male Caucasian and Asian neonates. In contrast, in female neonates, there was no significant difference (p = 0.099 and p = 0.07 for birthweight and calf circumference, respectively). In addition, while the slopes of the regression plots were not affected by gender in Asian newborns, there was a significant difference between male and female Caucasian newborns (p = 0.006 and p = 0.002 for birthweight and calf circumference, respectively). There was no significant correlation between cord leptin concentrations or anthropometric markers and steroid hormone concentrations. In conclusion, gender and ethnic differences in the relationship between leptin and anthropometric markers are detectable at birth between Asians and Caucasians, two ethnic groups that have been demonstrated to have different body compositions later in life. This may represent the first clinical evidence of a difference in leptin regulation between these two ethnic groups.

In adult male rats, selenium deficiency results in a near complete loss in the selenoprotein 5'-deiodinase in the liver, resulting in decreased peripheral deiodination of thyroxine (T4) and increased serum T4 concentrations. Serum 3,5,3'-triiodothyronine concentrations are normal or slightly decreased, and serum 3,3',5'-triiodothyronine concentrations are normal or slightly increased in selenium-deficient rats. We now report the effects of selenium deficiency on maternal and fetal thyroid hormone economy and on placental 5-deiodinase activity in the rat. Weanling female rats were fed either a selenium-deficient or selenium-supplemented diet for 4 wk before mating and then throughout gestation. Rats were killed at 21 d of gestation. Selenium deficiency was confirmed by a 95 and 94% decrease in glutathione peroxidase and a 84 and 56% decrease in liver type I outer ring 5' deiodinase activity in the mother and the fetus, respectively. In contrast to the increase in circulating T4 observed in selenium-deficient male and nonpregnant female adult rats, serum T4 was not affected by selenium deficiency in pregnant rats, but there was a 3-fold increase in serum 3,3',5'-triiodothyronine concentrations associated with a 70% decrease in maternal brain type II outer ring 5' deiodinase activity. Maternal serum 3,5,3'-triiodothyronine concentrations were decreased by 21%. Placental 5-deiodinase activity was unaffected by selenium deficiency. In the fetus, serum T4, 3,3',5'-triiodothyronine, and TSH concentrations were not affected by selenium deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)