Adiponectin: an intriguing hormone for paediatricians

Savino, Francesco; Petrucci, E.; Nanni, GE

doi:10.1111/j.1651-2227.2008.00750.x

Cited by 38 publications

(29 citation statements)

References 56 publications

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“…This model reveals a significant interaction between trunk adiposity index and adiponectin in the variation of average visfatin concentration. Currently, it is recognized that adiponectin concentrations are inversely proportional to body fat [45,46]. A possible explanation for this interaction may be attributed to reduction of adiponectin levels by increasing trunk fat in obese children, causing the variation of visfatin concentrations.…”

Section: Discussionmentioning

confidence: 99%

Resistin and visfatin concentrations are related to central obesity and inflammation in Brazilian children

Simões

Domingos

Oliveira

et al. 2018

Nutrire

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Background: The evidence that cardiovascular disease begins in childhood and adolescence, especially in the presence of excess weight, is associated with dysfunction on adipokine pro-inflammatory secretion. These affect glucose metabolism and lead to other complications related to insulin resistance and cardiovascular disease. This study assessed the association of anthropometric and metabolic parameters related to obesity, cardiovascular risk, and insulin resistance with concentrations of resistin and visfatin, in children. Methods: A cross-sectional study was developed with 178 children of 6-10 years old enrolled in public city schools. Anthropometric data, composition body, clinical, and biochemical were measured according to standard procedures. We used multiple regression models by stepwise method to evaluate the associations of resistin and visfatin with variables of interest. Results: In healthy weight children, resistin was associated with LDL cholesterol, visfatin, atherogenic index, and waist-to-height ratio, whereas in obese children resistin was associated with visfatin and interaction between conicity index and HOMA-AD. Furthermore, in healthy weight children, visfatin was associated to resistin and triceps skinfold thickness and negatively associated to HOMA-AD, while in obese ones visfatin was associated with waistto-height ratio, atherogenic index, resistin, and interaction between trunk adiposity index and adiponectin and was negatively associated with the HOMA-IR index. Conclusions: Our study shows an association between anthropometric and biochemical variables related to visceral fat and inflammation. These results suggest the resistin and visfatin as good pro-inflammatory markers. In addition, both adipokines are strongly related to central obesity, in children.

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Section: Discussionmentioning

confidence: 99%

Resistin and visfatin concentrations are related to central obesity and inflammation in Brazilian children

Simões

Domingos

Oliveira

et al. 2018

Nutrire

View full text Add to dashboard Cite

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“…In general, lower infant weights and leaner body compositions are associated with higher levels of adiponectin, at least through the first six months of life (Newburg et al 2010; but see Woo et al 2012). The fact that of adiponectin levels in breast milk can fluctuate with maternal energy balance and also in response to preterm or underweight infants suggests that it plays a key role in mediating the adaptive responses of infant adipose tissues (Savino et al 2008(Savino et al , 2010aWoo et al 2009). Adiponectin levels also correlate with linear growth, perhaps because adiponectin activates osteoblasts (Oshima et al 2005).…”

Section: Adiponectinmentioning

confidence: 99%

Mount Pinatubo, Inflammatory Cytokines, and the Immunological Ecology of Aeta Hunter-Gatherers

Bernstein

Dominy

2013

Human Biology

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Early growth cessation and reproduction are predicted to maximize fitness under conditions of high adult mortality, factors that could explain the pygmy phenotype of many rainforest hunter-gatherers. This lifehistory hypothesis is elegant but contentious in part because it lacks a clear biological mechanism. One mechanism stems from the field of human immunological ecology and the concept of inflammation "memory" across the life cycle and into subsequent generations. Maternal exposures to disease can infl uence immunological cues present in breast milk; because maternal provisioning via lactation occurs during critical periods of development, it is plausible that these cues can also mediate early growth cessation and small body size. Such epigenetic hypotheses are difficult to test, but the concept of developmental programming is attractive because it could explain how the stature of a population can change over time, in terms of both secular increases and rapid intergenerational decreases. Here we explore this concept by focusing on the Aeta, a population of former hunter-gatherers, and the Ilocano, a population of rice farmers. We predicted that Aeta mothers would produce breast milk with higher concentrations of four bioactive factors due to high infectious burdens. Further, we predicted that the concentrations of these factors would be highest in the cohort of women born in the early 1990s, when exposure to infectious disease was acute following the eruption of Mount Pinatubo in June 1991. We analyzed levels of adiponectin, C-reactive protein, and epidermal growth factor in the milk of 24 Aeta and 31 Ilocano women and found no detectable differences, whereas levels of transforming growth factor-β 2 were elevated among the Aeta, particularly as a function of maternal age. We found no difference between cohorts divided by the volcanic eruption (n = 43 born before, n = 12 born after). We discuss the implications of our findings for the terminal investment hypothesis and we suggest that the historical ecology of the Aeta is a promising model system for testing epigenetic hypotheses focused on the evolution of small body size. Abstract Early growth cessation and reproduction are predicted to maximize fitness under conditions of high adult mortality, factors that could explain the pygmy phenotype of many rainforest hunter-gatherers. This life-history hypothesis is elegant but contentious in part because it lacks a clear biological mechanism. One mechanism stems from the field of human immunological ecology and the concept of inflammation "memory" across the life cycle and into subsequent generations. Maternal exposures to disease can infl uence immunological cues present in breast milk; because maternal provisioning via lactation occurs during critical periods of development, it is plausible that these cues can also mediate early growth cessation and small body size. Such epigenetic hypotheses are difficult to test, but the concept of developmental programming is attractive because it could explain how the...

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“…Adiponectin increases fatty acid oxidation in adipose tissue, liver and muscle, enhancing insulin sensitivity, and inhibits inflammatory mediators and the expression of adhesion molecules within the vascular wall, lowering atherogenic risk (1,16). Adiponectin receptors have been identified predominantly in muscle (AdipoR1) and liver cells (AdipoR2), although in humans they are expressed ubiquitously in the body and brain (2,14,17). In most studies, circulating levels of leptin and adiponectin have been determined by enzyme-linked immunosorbent assays or enzyme immunoassay, or, alternatively, by radioimmunoassay (associated or not with in-house techniques).…”

Section: Leptin and Adiponectinmentioning

confidence: 99%