Journal of Pediatric Endocrinology and Metabolism 

About: Journal of Pediatric Endocrinology and Metabolism is an academic journal published by De Gruyter. The journal publishes majorly in the area(s): Diabetes mellitus & Medicine. It has an ISSN identifier of 0334-018X. Over the lifetime, 5440 publications have been published receiving 73873 citations. The journal is also known as: Journal of Pediatric Endocrinology & Metabolism.

Emergence of type 2 diabetes mellitus in children: epidemiological evidence.

Abstract: There have been numerous recent reports of case series of type 2 diabetes mellitus (DM) in American Indian, African-American, Hispanic, Asian-American and white children from North America. A similar phenomenon has also been described in several other countries. Prevalence and incidence estimates vary depending on the age and ethnicity of the population, but it is estimated that type 2 DM represents 8-45% of patients with DM currently diagnosed in large US pediatric centers; however, this is likely to be an underestimation and incidence is probably rising. The young patients diagnosed with type 2 DM in the USA were generally overweight, had a strong family history of type 2 DM and often had signs of insulin resistance. The majority belonged to ethnic groups at high risk for type 2 DM. More girls than boys were diagnosed. The few data on follow-up available suggest a high prevalence of microvascular and macrovascular complications among young adults who developed type 2 DM during childhood. Type 2 DM in children has recently been recognized as a potential public health problem in North America. As obesity is currently on the increase in several industrialized or industrializing countries, a similar increase in type 2 DM in children may soon emerge worldwide, and this will require preventative measures.

The "muscle-bone unit" in children and adolescents: a 2000 overview.

Abstract: In former views hormones, calcium, vitamin D and other humoral and nonmechanical agents dominated control of postnatal bone strength (and "mass") in children and adolescents. However later evidence that led to the Utah paradigm of skeletal physiology revealed that this control depends strongly on the largest mechanical loads on bones. Trauma excepted, muscles cause the largest loads and the largest bone strains, and these strains help to control the biological mechanisms that determine whole-bone strength. That makes the strength of children's load-bearing bones depend strongly on growing muscle strength and how bones respond to it. Most hormones and other nonmechanical agents that affect bone strength can help or hinder that "bone strength-muscle strength" relationship but cannot replace it. In addition some agents long thought to exert bone effects by acting directly on bone cells, affect muscle strength too. In that way they could affect bone strength indirectly. Such agents include growth hormone, adrenalcorticosteroid analogs, androgens, calcium, genes, vitamin D and its metabolites, etc. Thus bone and muscle do form a kind of operational unit. It is part of the Utah paradigm that supplements earlier views with later evidence and concepts. The paradigm explains how the "bone strength-muscle strength" relationship works. This article provides an overview of that physiology, and some of its implications for pediatric endocrinologists.

The roles of placental growth hormone and placental lactogen in the regulation of human fetal growth and development.

Abstract: The human growth hormone (hGH)/human placental lactogen (hPL) gene family, which consists of two GH and three PL genes, is important in the regulation of maternal and fetal metabolism and the growth and development of the fetus. During pregnancy, pituitary GH (hGH-N) expression in the mother is suppressed; and hGH-V, a GH variant expressed by the placenta, becomes the predominant GH in the mother. hPL, which is the product of the hPL-A and hPL-B genes, is secreted into both the maternal and fetal circulations after the sixth week of pregnancy. hGH-V and hPL act in concert in the mother to stimulate insulin-like growth factor (IGF) production and modulate intermediary metabolism, resulting in an increase in the availability of glucose and amino acids to the fetus. In the fetus, hPL acts via lactogenic receptors and possibly a unique PL receptor to modulate embryonic development, regulate intermediary metabolism and stimulate the production of IGFs, insulin, adrenocortical hormones and pulmonary surfactant. hGH-N, which is expressed by the fetal pituitary, has little or no physiological actions in the fetus until late in pregnancy due to the lack of functional GH receptors on fetal tissues. hGH-V, which is also a potent somatogenic hormone, is not released into the fetus. Taken together, studies of the hGH/hPL gene family during pregnancy reveal a complex interaction of the hormones with one another and with other growth factors. Additional investigations are necessary to clarify the relative roles of the family members in the regulation of fetal growth and development and the factors that modulate the expression of the genes.

Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility.

Abstract: Numerous studies have reported that offspring whose mothers had type 2 diabetes mellitus (DM) are more likely to develop type 2 DM, impaired glucose tolerance, and obesity at an early age than offspring whose fathers had DM. Exposure to the diabetic intrauterine environment has been shown to be an important risk factor for all these conditions. To what extent transmission of type 2 DM from mother to offspring is the effect of genetic inheritance and to what extent it is the long-term consequence of exposure to maternal hyperglycemia is still uncertain. There are, of course, interactions between the diabetic intrauterine environment and genetics. Several data in experimental animals as well as in humans suggest, however, that exposure of the fetus to the mother's DM confers a risk for type 2 DM and obesity that is above any genetically transmitted susceptibility. In the Pima Indian population much of the increase in childhood type 2 DM can be attributed to the diabetic intrauterine environment. This suggests that intensive glucose control during pregnancy might have extended beneficial effects, contributing to a decrease in the prevalence of childhood type 2 DM.

Type 2 diabetes mellitus in children and youth: a new epidemic.

Abstract: Type 2 diabetes mellitus (DM) has been described as a new epidemic affecting the American pediatric population. This is coincident with an overall 33% increase in DM prevalence documented during the last decade. In 1992, type 2 DM was a rare occurrence in most pediatric centers. By 1994, it represented up to 16% of new cases in urban areas, and by 1999, the incidence of new type 2 DM diagnoses ranged between 8% and 45%, depending on geographic location. These patients have been observed primarily in African American, Mexican American, Native American, and Asian American children and youth. As in the adult population, type 2 DM in children and youth occurs as a result of insulin resistance coupled with relative beta-cell failure. While there appears to be a host of potential genetic and environmental risk factors for these aberrations, perhaps the most significant risk factor is obesity. Other risk factors include a family history of type 2 DM, puberty, intrauterine exposure to DM, sedentary lifestyle, female gender, and certain ethnicities. To date, few studies have addressed the role of physical activity and nutrition counseling in improving glycemic outcome, the most effective ways to reduce cardiovascular risk, or the most effective treatment regimens for this population. Once type 2 DM is established, the persistence of obesity often interferes with the response to treatment and exacerbates the comorbidities of hypertension, dyslipidemia, atherosclerosis, and polycystic ovarian syndrome (PCOS). Since fewer than 10% of youth with type 2 DM can be treated with diet and exercise alone, pharmacological intervention is generally required to achieve normoglycemic targets. In most surveys, practitioners prescribe insulin or an oral agent, most often metformin. Specific treatment algorithms for pediatric patients with type 2 DM need to be rigorously investigated.