Metabolic syndrome and insulin resistance in pre-pubertal children with psoriasis.
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ABSTRACT:
SUBMITTER: Caroppo F
PROVIDER: S-EPMC8105196 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND: There are no data on the metabolic consequences of post-term birth (?42 weeks gestation). We hypothesized that post-term birth would adversely affect insulin sensitivity, as well as other metabolic parameters and body composition in childhood. METHODS: 77 healthy pre-pubertal children, born appropriate-for-gestational-age were studied in Auckland, New Zealand: 36 born post-term (18 boys) and 41 (27 boys) born at term (38-40 weeks gestation). Primary outcome was insulin sensitivity measured using intravenous glucose tolerance tests and Bergman's minimal model. Other assessments included fasting hormone concentrations and lipid profiles, body composition from whole-body dual-energy X-ray absorptiometry, 24-hour ambulatory blood pressure monitoring, and inflammatory markers. RESULTS: Insulin sensitivity was 34% lower in post-term than in term children (7.7 vs. 11.6 x10??·min?¹·(mU/l); p<0.0001). There was a compensatory increase in acute insulin response among post-term children (418 vs 304 mU/l; p=0.037), who also displayed lower glucose effectiveness than those born at term (2.25 vs 3.11 x10?²·min?¹; p=0.047). Post-term children not only had more body fat (p=0.014) and less fat-free mass (p=0.014), but also had increased central adiposity with more truncal fat (p=0.017) and greater android to gynoid fat ratio (p=0.007) compared to term controls. Further, post-term children displayed other markers of the metabolic syndrome: lower normal nocturnal systolic blood pressure dipping (p=0.027), lower adiponectin concentrations (p=0.005), as well as higher leptin (p=0.008) and uric acid (p=0.033) concentrations. Post-term boys (but not girls) also displayed a less favourable lipid profile, with higher total cholesterol (p=0.018) and LDL-C (p=0.006) concentrations, and total cholesterol to HDL-C ratio (p=0.048). CONCLUSIONS: Post-term children have reduced insulin sensitivity and display a number of early markers of the metabolic syndrome. These findings could have important implications for the management of prolonged pregnancies. Future studies need to examine potential impacts later in life, as well as possible underlying mechanisms.
| S-EPMC3698136 | biostudies-literature
Project description:Insulin resistance and the metabolic syndrome are complex metabolic traits and key risk factors for the development of cardiovascular disease. They result from the interplay of environmental and genetic factors but the full extent of the genetic background to these conditions remains incomplete. Large-scale genome-wide association studies have helped advance the identification of common genetic variation associated with insulin resistance and the metabolic syndrome, and more recently, exome sequencing has allowed the identification of rare variants associated with the pathogenesis of these conditions. Many variants associated with insulin resistance are directly involved in glucose metabolism; however, functional studies are required to assess the contribution of other variants to the development of insulin resistance. Many genetic variants involved in the pathogenesis of the metabolic syndrome are associated with lipid metabolism.
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Project description:Sepsis is a common and deadly syndrome in which a dysregulated host response to infection causes organ failure and death. The current lack of treatment options suggests that a new approach to studying sepsis is needed. Pre-pubertal children show a relative resistance to death from severe infections and sepsis. To explore this phenomenon experimentally, we used an endotoxemia model of sepsis in mice. Following intra-peritoneal injection of endotoxin, pre-pubertal mice showed greater survival than post-pubertal mice (76.3% vs. 28.6%), despite exhibiting a similar degree of inflammation after two hours. Age-associated differences in the inflammatory response only became evident at twenty hours, when post-pubertal mice showed prolonged elevation of serum cytokines and differential recruitment of peritoneal immune cells. Mechanistically, prevention of puberty by hormonal blockade or acceleration of puberty by oestrogen treatment led to increased or decreased survival from endotoxemia, respectively. Additionally, the adoptive transfer of pre-pubertal peritoneal cells improved the survival of post-pubertal recipient mice, while post-pubertal peritoneal cells or vehicle did not. These data establish a model for studying childhood resistance to mortality from endotoxemia, demonstrate that oestrogen is responsible for an increased susceptibility to mortality after puberty, and identify peritoneal cells as mediators of pre-pubertal resistance.
| S-EPMC5707402 | biostudies-literature
Project description:BACKGROUND/OBJECTIVES:Neuroimaging investigations of brain pathways involved in reward and motivation have primarily focused on adults. This study sought to identify brain responses to visual food cues and explore its relationships with adiposity and sex in pre-pubertal children. METHODS:Brain responses to palatable food vs. non-food cues were measured in 53 children (age: 8.18 ± .66 years; sex: 22 boys, 31 girls) after an overnight fast. Whole-brain analysis (cluster-correction Z > 2.3, P < .05) was performed to examine brain food cue reactivity and its relationships with adiposity and sex. RESULTS:Greater brain activity in response to food vs. non-food cues was observed in regions implicated in reward (orbital frontal cortex, striatum), taste (insula, postcentral gyrus), appetite (hypothalamus), emotion (amygdala), memory (hippocampus), visual processing (occipital cortex) and attention (parietal cortex). A negative association was found between percent body fat and food cue reactivity in the medial prefrontal cortex and lateral orbital frontal cortex adjusting for age and sex. Boys compared with girls had increased food cue reactivity in right hippocampus and visual cortex. CONCLUSIONS:These data suggest that body fat and sex are important moderators of brain food cue reactivity in children.
| S-EPMC6336530 | biostudies-literature
Project description:Obesity and its consequent complications such as hypertension and metabolic syndrome are increasing in incidence in almost all countries. Insulin resistance is common in obesity. Renin- angiotensin system (RAS) is an important target in the treatment of hypertension and drugs that act on RAS improve insulin resistance and decrease the incidence of type 2 diabetes mellitus, explaining the close association between hypertension and type 2 diabetes mellitus. RAS influences food intake by modulating the hypothalamic expression of neuropeptide Y and orexins via AMPK dephosphorylation. Estrogen reduces appetite by its action on the brain in a way similar to leptin, an anorexigenic action that seems to be mediated via hypothalamic pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and synaptic plasticity in the arcuate nucleus similar to leptin. Estrogen stimulates lipoxin A4, a potent vasodilator and platelet anti-aggregator. Since both RAS and estrogen act on the hypothalamic neuropeptides and regulate food intake and obesity, it is likely that RAS modulates LXA4 synthesis. Thus, it is proposed that Angiotensin-II receptor blockers and angiotensin-converting enzymes and angiotensin-II antagonists may have the ability to augment LXA4 synthesis and thus bring about their beneficial actions.
| S-EPMC5290902 | biostudies-literature
Project description:OBJECTIVES: To investigate the prevalence of non-alcoholic fatty liver disease (NAFLD) in children and its relationship to metabolic syndrome, insulin resistance, and waist circumference (WC). METHODS: This was a population-based cross-sectional, case-control study. Cases were selected among students of a primary and junior high school, respectively, and age- and sex-matched control subjects were selected randomly (ratio of cases to control subject was 37:113). RESULTS: Of the 846 students, aged between 6 and 15 years, enrolled in the study and screened by ultrasonography, 37 children were diagnosed as having NAFLD (score >/= 1). There was a significant sex difference in the prevalence of NAFLD(P = 0.003). The trend test revealed a strong dose-response relationship (P < 0.001) between pediatric NAFLD and the number of the proposed components of pediatric metabolic syndrome in Japan (MetS-JC), such as a clustering of the components of MetS-JC. Additionally, the linear trend of the odds ratios (ORs) with increasing percentile of the homeostasis model assessment-insulin resistance (HOMA-IR) was statistically significant (P < 0.001). However, when WC was added to the logistic model, the ORs were no longer significant, whereas WC turned out to be an independent risk factor for NAFLD regardless of the HOMA-IR index. CONCLUSION: The prevalence of NAFLD in children and adolescents is closely related to metabolic syndrome, insulin resistance, and WC.
| S-EPMC2684773 | biostudies-other
Project description:In view of the high incidence of metabolic syndrome and the role of exercise in promoting metabolic disorders, the present study aimed to investigate the therapeutic effects of swimming intervention on metabolic syndrome. In the present study, a total of 100 patients with metabolic syndrome and 100 healthy individuals were included. Fasting blood was extracted from each participant, and the serum levels of interleukin (IL)-1, high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor ? (TNF-?) and IL-8 were measured by sandwich enzyme-linked immunosorbent assay. Patients were randomly divided into five groups (groups A-E). Patients in group A was treated with conventional drug treatment. Besides conventional treatment, patients in groups B-E were also subjected to swimming intervention for 15, 30, 45 and 60 min each time, respectively, four times a week for 3 months. Changes in the homeostatic model assessment of ?-cell function and insulin resistance (HOMA-IR) score, and in the serum levels of IL-1, hs-CRP, TNF-? and IL-8 were recorded. Furthermore, muscle tissues were collected from patients, and the expression levels of insulin receptor substrate-1 (IRS-1), glucose transporter type 4 (GLUT4) and protein kinase B (Akt) in the tissues were detected by western blot assay. The results revealed that HOMA-IR and the serum levels of IL-1, hs-CRP, TNF-? and IL-8 were significantly higher in metabolic syndrome patients as compared with those in the normal controls, while swimming intervention reduced HOMA-IR and these serum levels to different extents. Swimming intervention also promoted IRS-1 and Akt phosphorylation, and increased GLUT4 expression level. Thus, it is concluded that swimming intervention may improve metabolic syndrome through multiple pathways.
| S-EPMC6307524 | biostudies-other
Project description:UnlabelledAims/Introduction:? It is important to identify individuals at risk of metabolic syndrome (MetS), namely those with insulin resistance. Therefore, the aim of the present study was to find anthropometric and metabolic parameters that can better predict insulin resistance.Subjects and methods? We selected 3899 individuals (2058 men and 1841 women), excluding those with fasting plasma glucose (FPG) ?126?mg/dL, on medication for hypertension, dyslipidemia or diabetes, and those with a history of advanced macrovascular disease. Using multivariate analyses, we selected components for obesity, lipids, and blood pressure based on the strength of their association with the homeostasis model assessment of insulin resistance (HOMA-IR).Results? In multiple linear regression analysis, body mass index (BMI), waist circumference (WC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and systolic blood pressure (SBP) were selected in men and women, and the effect of BMI on HOMA-IR outweighed that of WC. In multiple logistic regression analysis, BMI, TG, and SBP were significantly associated with HOMA-IR ?2.5 in both genders, but WC and HDL-C were only selected in men. Combinations of BMI, TG, SBP, and FPG showed higher HOMA-IR values than those of the existing MetS components, considered useful for the identification of individual with higher insulin resistance.Conclusions? Body mass index, TG and SBP were selected as components significantly related to insulin resistance. The selected components were fundamentally adherent to the existing MetS criteria, the only difference being the measure of obesity, in which a stronger association with insulin resistance was observed for BMI than WC. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00162.x, 2011).
| S-EPMC4020738 | biostudies-literature
Project description:Metabolic syndrome (MetS) is a major public health burden worldwide and associated with brain abnormalities. Although insulin resistance is considered a pivotal feature of MetS, its role in the pathogenesis of MetS-related brain alterations in the general population is unclear. Therefore, in 973 participants (mean age 52.5 years) of the population-based Rhineland Study, we assessed brain morphology in relation to MetS and insulin resistance, and evaluated to what extent the pattern of structural brain changes seen in MetS overlap with those associated with insulin resistance. Cortical reconstruction and volumetric segmentation were obtained from high-resolution brain images at 3 Tesla using FreeSurfer. The relations between metabolic measures and brain structure were assessed through (generalized) linear models. Both MetS and insulin resistance were associated with smaller cortical gray matter volume and thickness, but not with white matter or subcortical gray matter volume. Age- and sex-adjusted vertex-based brain morphometry demonstrated that MetS and insulin resistance were related to cortical thinning in a similar spatial pattern. Importantly, no independent effect of MetS on cortical gray matter was observed beyond the effect of insulin resistance. Our findings suggest that addressing insulin resistance is critical in the prevention of MetS-related brain changes in later life.
| S-EPMC8090787 | biostudies-literature
Project description:ObjectiveWe assessed the sex-specific differences in the molecular mechanisms of insulin resistance in muscle and adipose tissue, in a MS rat model induced by a high sucrose diet.MethodsMale, female, and ovariectomized female Wistar rats were randomly distributed in control and high-sucrose diet (HSD) groups, supplemented for 24 weeks with 20% sucrose in the drinking water. At the end, we assessed parameters related to MS, analyzing the effects of the HSD on critical nodes of the insulin signaling pathway in muscle and adipose tissue.ResultsAt the end of the treatment, HSD groups of both sexes developed obesity, with a 15, 33 and 23% of body weight gain in male, female, and OVX groups respectively, compared with controls; mainly related to hypertrophy of peripancreatic and gonadal adipose tissue. They also developed hypertriglyceridemia, and liver steatosis, with the last being worse in the HSD females. Compared to the control groups, HSD rats had higher IL1B and TNFA levels and insulin resistance. HSD females were more intolerant to glucose than HSD males. Our observations suggest that insulin resistance mechanisms include an increase in phosphorylated AKT(S473) form in HSD male and female groups and a decrease in phosphorylated P70S6K1(T389) in the HSD male groups from peripancreatic adipose tissue. While in gonadal adipose tissue the phosphorylated form of AKT decreased in HSD females, but not in HSD males. Finally, HSD groups showed a reduction in p-AKT levels in gastrocnemius muscle.ConclusionA high-sucrose diet induces MS and insulin resistance with sex-associated differences and in a tissue-specific manner.
| S-EPMC7583132 | biostudies-literature