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      The Influence of Obesity on Puberty and Insulin Resistance in Mexican Children

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          Abstract

          Obesity is considered the main risk factor associated with the development of insulin resistance (IR). The aim of this study was to evaluate the influence of obesity on puberty onset and IR in Mexican children. A total of 378 children (189 boys and 189 girls) aged 8–14 years participated in the study. IR was estimated using the homeostasis model assessment for IR (HOMA-IR). The mean fasting glucose (FG) and basal insulin levels were 82 mg/dl and 11.0 μIU/ml in boys and 77.3 mg/dl and 12.3 μIU/ml in girls ( P < 0.05). Subjects with obesity at Tanner stages II–V showed increased FG levels ( P < 0.05). In boys with obesity, there was a decrease in HOMA-IR in Tanner stage IV and differences in age between boys with normal weight and those with obesity in Tanner V, being older the boys with obesity. Obesity in children and adolescents was associated with higher HOMA-IR values. In boys with obesity, IR increased at the end of pubertal maturation, with a delay in puberty. These findings should be considered on the establishment of IR cutoff values for pubertal population in Mexico and in the establishment of strategies to prevent the health problems related to obesity.

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          The assessment of insulin resistance in man.

          Insulin resistance exists when a normal concentration of insulin produces a less than normal biological response. The ability to measure insulin resistance is important in order to understand the aetiopathology of Type 2 diabetes, to examine the epidemiology and to assess the effects of intervention. We assess and compare methods of measurement and have undertaken a literature review from 1966 to 2001. Quantitative estimates of insulin resistance can be obtained using model assessments, clamps or insulin infusion sensitivity tests. There is considerable variation in the complexity and labour intensity of the various methods. The most well-established methods are the euglycaemic clamp, minimal model assessment and homeostatic model assessment (HOMA). No single test is appropriate under all circumstances. There are a number of well-established tests used to measure insulin resistance: the choice of method depends on the size and type of study to be undertaken. Although the so-called 'gold-standard' test, the euglycaemic clamp, is useful for intensive physiological studies on small numbers of subjects, a simpler tool such as HOMA is more appropriate for large epidemiological studies. It is important to be aware that most techniques measure stimulated insulin resistance whereas HOMA gives an estimate of basal insulin resistance. Caution should be exercised when making comparisons between studies due to variations in infusion protocols, sampling procedures and hormone assays used in different studies.
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            Limitations in the Use of Indices Using Glucose and Insulin Levels to Predict Insulin Sensitivity

            OBJECTIVE To examine the utility of commonly used insulin sensitivity indices in nondiabetic European Americans (EAs) and African Americans (AAs). RESEARCH DESIGN AND METHODS Two-hundred forty nondiabetic participants were studied. Euglycemic-hyperinsulinemic clamp was the gold standard approach to assess glucose disposal rates (GDR) normalized by lean body mass. The homeostatic model assessment for insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were calculated from fasting plasma glucose and insulin (FIL). Oral glucose tolerance test (OGTT) was performed to determine Matsuda index, the simple index assessing insulin sensitivity (SIisOGTT), Avignon index, and Stomvoll index. Relationships among these indices with GDR were analyzed by multiple regression. RESULTS GDR values were similar in EA and AA subgroups; even so, AA exhibited higher FIL and were insulin-resistant compared with EA, as assessed by HOMA-IR, QUICKI, Matsuda index, SIisOGTT, Avignon index, and Stumvoll index. In the overall study population, GDR was significantly correlated with all studied insulin sensitivity indices (/r/ = 0.381–0.513); however, these indices were not superior to FIL in predicting GDR. Race and gender affected the strength of this relationship. In AA males, FIL and HOMA-IR were not correlated with GDR. In contrast, Matsuda index and SIisOGTT were significantly correlated with GDR in AA males, and Matsuda index was superior to HOMA-IR and QUICKI in AAs overall. CONCLUSIONS Insulin sensitivity indices based on glucose and insulin levels should be used cautiously as measures of peripheral insulin sensitivity when comparing mixed gender and mixed race populations. Matsuda index and SIisOGTT are reliable in studies that include AA males.
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              Sexual differentiation, pregnancy, calorie restriction, and aging affect the adipocyte-specific secretory protein adiponectin.

              Adiponectin or adipocyte complement-related protein of 30 kDa (Acrp30) is a circulating protein produced exclusively in adipocytes. Circulating Acrp30 levels have been associated with insulin sensitivity in adult mice and humans, yet the Acrp30 profile over the lifespan and its hormonal regulation in vivo have not been previously described. Hence, we set forth to determine whether hormonal and metabolic changes associated with sexual maturation, reproduction, aging, and calorie restriction affect Acrp30. In mice, Acrp30 levels increase during sexual maturation by 4-fold in males and 10-fold in females. Neonatal castration (CX) allows Acrp30 of adults to reach female levels. CX in adults does not lead to female Acrp30 levels unless glucocorticoid exposure is elevated simultaneously by implant. Ovariectomy of infant mice does not interfere with the pubertal rise of Acrp30. However, ovariectomy in adults increases Acrp30. Estrogen suppressed Acrp30 in mice and 3T3-L1 adipocytes. In parallel to changes in estrogen action, Acrp30 decreased in late gestation but increased in both calorie-restricted and old (anovulatory) mice. The reduction of Acrp30 in lactating dams is consistent with a suppressive effect of prolactin and a stimulating effect of bromocriptine. In summary, Acrp30 levels in serum are under complex hormonal control and may play a key role in determining systemic insulin sensitivity under the respective conditions.
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                Author and article information

                Contributors
                Journal
                Int J Endocrinol
                Int J Endocrinol
                IJE
                International Journal of Endocrinology
                Hindawi
                1687-8337
                1687-8345
                2018
                3 September 2018
                : 2018
                : 7067292
                Affiliations
                1Hospital General Zacatecas “Luz González Cosío”, Servicios de Salud de Zacatecas, Zacatecas, 98160 ZAC, Mexico
                2Molecular Medicine Laboratory, Unidad Academica de Medicina Humana y C.S., Universidad Autonoma de Zacatecas, Zacatecas, 98160 ZAC, Mexico
                3Unidad Academica de Ingenieria Electrica, Universidad Autonoma de Zacatecas, Zacatecas, 98160 ZAC, Mexico
                4Servicio de Endocrinologia Pediatrica, Hospital General “Gaudencio González Garza, ” Centro Medico Nacional La Raza, Instituto Mexicano del Seguro Social (IMSS), 02990 Ciudad de Mexico, Mexico
                5Unidad Academica de Enfermeria, Universidad Autonoma de Zacatecas, Zacatecas, 98160 ZAC, Mexico
                Author notes

                Academic Editor: Javier Salvador

                Author information
                http://orcid.org/0000-0002-6307-1696
                http://orcid.org/0000-0002-7635-4687
                http://orcid.org/0000-0003-1478-9068
                Article
                10.1155/2018/7067292
                6140127
                fadc1878-e2ad-4cd7-8b8b-4cd4f749ab4d
                Copyright © 2018 Edith Cardenas-Vargas et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 February 2018
                : 13 June 2018
                Funding
                Funded by: ICP
                Funded by: Consejo Nacional de Ciencia y Tecnología
                Award ID: 2014-01-225520
                Award ID: 2015-01-254106
                Award ID: 2015-258316
                Award ID: 2016-01-273144
                Funded by: PDCPN
                Award ID: 2015-01-63
                Categories
                Research Article

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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