WHAT'S KNOWN ON THIS SUBJECT:There has been a dramatic increase in the use of adolescent bariatric surgery. However, previous studies were unable to distinguish laparoscopic versus open procedures. Furthermore, the use of laparoscopic adjustable gastric banding (LAGB) has not been studied on a population level. WHAT THIS STUDY ADDS:The rate of LAGB increased sevenfold from 2005 to 2007 with a corresponding decrease in the rate of laparoscopic Roux-en-Y gastric bypass. Furthermore, white adolescents represented only 28% of those who were overweight but accounted for 65% of the procedures.abstract OBJECTIVE: The goal of this study was to evaluate trends, and outcomes of adolescents who undergo bariatric surgery. PATIENTS AND METHODS: RESULTS:Overall, 590 adolescents (aged 13-20 years) underwent bariatric surgery in 86 hospitals. White adolescents represented 28% of those who were overweight but accounted for 65% of the procedures. Rates of laparoscopic adjustable gastric banding (LAGB) increased 6.9-fold from 0.3 to 1.5 per 100 000 population (P Ͻ .01), whereas laparoscopic Roux-en-Y gastric bypass (LRYGB) rates decreased from 3.8 to 2.7 per 100 000 population (P Ͻ .01). Self-payers were more likely to undergo LAGB (relative risk [RR]: 3.51 [95% confidence interval: 2.11-5.32]) and less likely to undergo LRYGB (RR: 0.45 [95% confidence interval: 0.33-0.58]) compared with privately insured adolescents. The rate of major in-hospital complication was 1%, and no deaths were reported. Of the patients who received LAGB, 4.7% had band revision/removal. In contrast, 2.9% of those who received LRYGB required reoperations. CONCLUSIONS:White adolescent girls disproportionately underwent bariatric surgery. Although LAGB has not been approved by the US Food and Drug Administration for use in children, its use has increased dramatically. There was a complication rate and no deaths. Long-term studies are needed to fully assess the efficacy, safety, and health care costs of these procedures in adolescents.

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Our study demonstrates that rapidly achieving and sustaining almost universal ITN usage rates is possible using a community-based approach. Closing the gap between ITN ownership and use will help communities to realize the full potential of ITNs in the prevention of malaria.

Leptin is a secretory product of adipocytes that has been shown to affect food intake, metabolism, and reproduction. One site of leptin's action is the central nervous system, where the leptin receptor (Ob-R) messenger ribonucleic acid (mRNA) and protein are expressed in discrete areas. In both the rat and monkey, Ob-R mRNA has been localized in the Raphe nuclei of the brainstem. Neurons in the Raphe nuclei are the primary source of serotonin in the brain. Serotonergic pathways influence both feeding and reproduction, and these cells are plausible direct targets for leptin's action. We used double label in situ hybridization and computerized image analysis to determine whether serotonergic neurons in the brainstem of the female pigtailed macaque (Macaca nemestrina) express Ob-R mRNA. We observed that many cells in the Raphe nuclei express serotonin transporter mRNA, a marker of serotonergic cells, and Ob-R mRNA. Based on quantitative analysis, the highest number of cells that express both serotonin transporter and Ob-R mRNAs were found in the caudal dorsal Raphe and median Raphe nuclei; fewer double labeled cells were situated in the caudal linear nucleus and rostral median Raphe, whereas double labeled cells occurred infrequently in the rostral dorsal Raphe. These observations suggest that leptin may act on serotonergic cells to mediate some of its effects on ingestive behavior, metabolism, and reproduction. (J Clin Endocrinol Metab 86: [422][423][424][425][426] 2001) L EPTIN IS A protein product of the obese (ob) gene and is secreted primarily by adipocytes. Leptin regulates body weight and metabolism and may also act as a metabolic signal to the reproductive axis (1, 2). Animals that have mutations in the genes that code for either leptin (e.g. ob/ob mice) or its receptor (Ob-R; e.g. db/db mice and fa/fa rats) are hyperphagic, obese, and infertile (3, 4). These abnormalities are corrected in ob/ob mice by treatment with exogenous leptin (5, 6). In rodents as well as nonhuman primates, central injections of leptin result in decreased food intake (6, 7), suggesting that leptin acts directly on the brain to regulate this physiological process. Fasting results in a decline in circulating leptin levels (8) as well as a reduction in the activity of the neuroendocrine reproductive axis, as evidenced by a decrease in plasma levels of LH (9, 10). Both central and peripheral administration of leptin to fasted animals prevents the suppression of LH secretion (11-13).Although it would appear that leptin acts on the brain to affect feeding and reproduction, the neural circuitry mediating leptin's action in the central nervous system has yet to be fully elucidated. To date, the majority of effort in mapping this circuitry has focused on the hypothalamus, an area of the brain known to be involved in the regulation of ingestive behaviors, metabolism, and reproduction (14). This is due to the abundant expression of Ob-R messenger ribonucleic acid (mRNA) in several hypothalamic nuclei (12,15). Recently, we identifie...

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