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Introduction: Obesity and metabolic syndrome (MetS) have immediate and long-term consequences on adolescent health and well-being. Among the available treatments for MetS in adolescents, behavioral interventions such as increasing physical activity (PA) are preferred. This study aimed to investigate the association of PA and sitting time with MetS and a complete set of metabolic health parameters. Methods: Data from the Pediatric Brazilian Metabolic Syndrome Study (BRAMS-P), a cross-sectional multicenter study conducted using a convenience sample of 448 Brazilian adolescents (10y-19y), were used. Sociodemographic and lifestyle information were collected using a standardized questionnaire. Daily PA and sitting time were estimated from the International PA Questionnaire. Anthropometric parameters, body composition, and blood pressure were measured by trained researchers. Blood lipids, uric acid, hepatic enzymes, creatinine, glycated hemoglobin, glucose, and insulin were measured in fasting blood samples, and the Homeostasis Model Assessment for Insulin Resistance was calculated. A subsample of 57 adolescents underwent the hyperglycemic clamp protocol. Results: The odds for metabolic syndrome were higher among adolescents who spent >8h sitting (OR (95%CI)=2.11 (1.02 - 4.38)), but not in those classified as active (OR (95%CI)=0.98 (0.42 - 2.26)). Adolescents who spent more time sitting had higher BMI, waist circumference, sagittal abdominal diameter, neck circumference, percentage of body fat, and worse blood lipid profile. The insulin sensitivity index was moderately and positively correlated with moderate-to-high PA in minutes per day (rho=0.29; p=0.047). Conclusion: Time spent sitting was associated with worse metabolic parameters and must be restricted in favor of adolescent health. Regular PA is associated with improved insulin sensitivity and may be encouraged not only in adolescents with obesity or metabolic disorders but also to prevent adverse metabolic outcomes in normal-weight adolescents.
Assuntos
Resistência à Insulina , Síndrome Metabólica , Humanos , Adolescente , Criança , Resistência à Insulina/fisiologia , Estudos Transversais , Obesidade/complicações , Lipídeos , Exercício FísicoRESUMO
Background: Appetite disorders are frequent and scantly studied in peritoneal dialysis (PD) patients and are associated with malnutrition and cardiovascular complications. Objective: We investigated the relationship between uremic insulin resistance, pro-inflammatory cytokines, and appetite-related peptides release (ARPr) with eating-behavior disorders in PD patients. Methods: We included 42 PD patients (12 suffering anorexia, 12 obese with high food-intake, and 18 asymptomatic) and 10 controls. We measured blood levels of ARPr including orexigens [neuropeptide-Y (NPY), ghrelin, and nitric-oxide], anorexigens [cholecystokinin, insulin, corticotropin-releasing factor, leptin, and adiponectin (Ad)], and cytokines (TNF-α, sTNFα-R2, and IL-6) both at baseline and after administering a standard-food stimulus (SFS). We also measured the expression of TNF-α, leptin and Ad-encoding mRNAs in abdominal adipose tissue. We compared these markers with eating motivation measured by a Visual Analog Scale (VAS). Results: Anorexics showed both little appetite, measured by a VAS, and low levels of orexigens that remained constant after SFS, coupled with high levels of anorexigens at baseline and after SFS. Obeses showed higher appetite, increased baseline levels of orexigens, lower baseline levels of anorexigens and cytokines and two peaks of NPY after SFS. The different patterns of ARPr and cytokines pointed to a close relationship with uremic insulin resistance. In fact, the euglycemic-hyperglycemic clamp reproduced these disorders. In anorexics, TNF-α fat expression was increased. In obese patients, leptin expression in fat tissue was down-regulated and showed correlation with the appetite. Conclusion: In PD, appetite is governed by substances that are altered at baseline and abnormally released. Such modulators are controlled by insulin metabolism and cytokines and, while anorexics display inflammatory predominance, obese patients predominantly display insulin resistance.
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BACKGROUND: We aimed to assess the long-term outcomes of biliopancreatic diversion (BPD) surgery on glycemic control, insulin sensitivity (IS), and beta cell function using complementary oral and intravenous dynamic tests. METHODS: A total of 57 women were divided into three groups: 19 lean, 18 obese (both groups with normal glucose tolerance (NGT)), and 20 obese with type 2 diabetes who underwent BPD and were reassessed 12 months after the procedure. OGTTs and hyperglycemic clamps (HG) were performed. Mathematical modeling was used to analyze IS, beta cell function, and delayed time of beta cell response. The basal, dynamic (first phase/steps of insulin secretion), and static (second phase/steps of insulin secretion) disposition indexes were calculated. RESULTS: After surgery, the patients exhibited improvements in glycemic control and 15 patients achieved diabetes remission. The surgical patients demonstrated normalized IS in OGGT and HG tests compared to the control groups. The basal beta cell function was improved but remained impaired compared to the Lean NGT group. The stimulated beta cell function parameters showed marked improvements regarding the intravenous stimulus and the second phase/distal steps of insulin secretion. The delay time markedly decreased and became normalized in both dynamic tests. CONCLUSIONS: The common physiopathology features of type 2 diabetes, i.e., impaired IS and beta cell dysfunction, were demonstrated to be primarily functional and were likely to be reversible to some degree after the BPD. The marked long-term improvement in glycemic control after BPD was closely related to IS improvement and mainly by the recovery of several beta cell physiological features.
Assuntos
Desvio Biliopancreático , Glicemia/metabolismo , Diabetes Mellitus Tipo 2/cirurgia , Resistência à Insulina/fisiologia , Células Secretoras de Insulina/metabolismo , Obesidade/cirurgia , Adulto , Diabetes Mellitus Tipo 2/metabolismo , Feminino , Glucose/metabolismo , Teste de Tolerância a Glucose , Humanos , Insulina/metabolismo , Pessoa de Meia-Idade , Obesidade/metabolismoRESUMO
We evaluated changes in glucose tolerance of 17 progressors and 62 non-progressors for 9 years to improve our understanding of the pathogenesis of type 2 diabetes mellitus. Changes in anthropometric measurements and responses to an oral glucose tolerance test (OGTT) were analyzed. We identified 14 pairs of individuals, one from each group, who were initially normal glucose tolerant and were matched for gender, age, weight, and girth. We compared initial plasma glucose and insulin curves (from OGTT), insulin secretion (first and second phases) and insulin sensitivity indices (from hyperglycemic clamp assay) for both groups. In the normal glucose tolerant phase, progressors presented: 1) a higher OGTT blood glucose response with hyperglycemia in the second hour and a similar insulin response vs non-progressors; 2) a reduced first-phase insulin secretion (2.0 ± 0.3 vs 2.3 ± 0.3 pmol/L; P < 0.02) with a similar insulin sensitivity index and a lower disposition index (3.9 ± 0.2 vs 4.1 ± 0.2 µmol·kg-1·min-1 ; P < 0.05) vs non-progressors. After 9 years, both groups presented similar increases in weight and fasting blood glucose levels and progressors had an increased glycemic response at 120 min (P < 0.05) and reduced early insulin response to OGTT (progressors, 1st: 2.10 ± 0.34 vs 2nd: 1.87 ± 0.25 pmol/mmol; non-progressors, 1st: 2.15 ± 0.28 vs 2nd: 2.03 ± 0.39 pmol/mmol; P < 0.05). Theses data suggest that β-cell dysfunction might be a risk factor for type 2 diabetes mellitus.