Insulin Sensitivity

Source: www.ncbi.nlm.nih.gov --- 32 days ago
Related Articles Increased energy expenditure and Insulin Sensitivity in the high bone mass {Delta}FosB transgenic mice. Endocrinology. 2008 Sep 4; Authors: Rowe GC, Choi CS, Neff L, Horne WC, Shulman GI, Baron R Obesity and osteoporosis are major health issue affecting millions of individuals. Transgenic mice overexpressing DeltaFosB, an AP-1 transcription factor, under the control of the enolase 2 (ENO2) promoter exhibit both an increase in bone density and a decrease in adipose mass. Here, we demonstrate that DeltaFosB overexpression increases fatty-acid oxidation and energy expenditure, leading to a decrease in adipocyte size and adipose mass. In addition, the ENO2-DeltaFosB mice exhibit increased Insulin Sensitivity and glucose tolerance. Targeted overexpression of DeltaFosB in adipocytes using the aP2 promoter failed to induce changes in fat or in bone, showing that the effect on metabolic activity is not due to cell-autonomous effects of DeltaFosB within adipocytes. Detailed analysis of the ENO2-DeltaFosB mice demonstrated that energy expenditure was increased in muscle, independent of locomotor activity. These findings provide evidence that signaling downstream of DeltaFosB is a potential target not only for osteoporosis but also for obesity and diabetes. PMID: 18772235 [PubMed - as supplied by publisher] ...

Source: www.ncbi.nlm.nih.gov --- 1 day ago
[The effect of short-time continuous positive airway pressure treatment on Insulin Sensitivity in patients with obstructive sleep apnea-hypopnea syndrome and type 2 diabetes] Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2008 Jul;22(13):597-9 Authors: Wang H, Wang L, Liu J OBJECTIVE: To investigate the effects of short-time continuous positive airway pressure treatment before the surgery on Insulin Sensitivity in patients with obstructive sleep apnea-hypopnea syndrome and type 2 diabetes who need the operation of uvulopalatophargngoplasty. METHOD: Thirty cases of patients with moderate and severe obstructive sleep apnea-hypopnea syndrome and type 2 diabetes who need the operation of UPPP were included in this study. The apnea hypopnea index (AHI) and LSaO2 and the Insulin Sensitivity index (ISI) was evaluated by homeostasis model assessment (HOMA), after 7 days of effective CPAP treatment. Subsequently, the data of the PSG and the ISI were rechecked and compared to the data previously achieved. RESULT: After 7 days of effective CPAP treatment, the level of AHI and LSaO2 changed (P < 0.05). The level of ISI improved (P < 0.05), while the level of AHI was correlated with fasting blood Insulin level (r = 0.6365, P < 0.05) and was inverse correlated with Insulin Sensitivity (r = - 0.6229, P < 0.05). There was an negative correlation between LSaO2 and fasting blood Insulin level (r = -0.8889, P < 0.05), and there was a correlation between ...

Source: www.ncbi.nlm.nih.gov --- 7 days ago
Related Articles The effect of metformin on measurements of Insulin Sensitivity and beta cell response in 18 horses and ponies with Insulin resistance. Equine Vet J. 2008 Jul;40(5):493-500 Authors: Durham AE, Rendle DI, Newton JE REASONS FOR PERFORMING STUDY: Laminitis in equids is a very common debilitating disease, and Insulin resistance (IR) and hyperinsulinaemia are increasingly recognised as important predisposing factors. Pharmacological modification of IR and hyperinsulinaemia might reduce the risk of laminitis. HYPOTHESIS: Metformin, a drug commonly prescribed for treatment of human IR, may also decrease IR in equids. METHODS: Eighteen horses and ponies with IR and recurrent laminitis were treated with 15 mg/kg bwt metformin per os q. 12 h. Each animal served as its own control by comparing pre- and post treatment proxies for IR, Insulin Sensitivity (IS) and pancreatic beta cell function while controlling for possible dietary and managemental influences on IR. RESULTS: Evidence of significantly improved IS and decreased pancreatic beta cell secretion was found following metformin treatment. The magnitude of effect was greater at earlier resampling (6-14 days) than at later times (23-220 days). Apparent subjective clinical benefits were good but less favourable than effects on IR. CONCLUSIONS: Metformin is safe and appears to increase IS in equids. POTENTIAL RELEVANCE: Metformin may be indicated as a treatment for IR in equids. ...

Source: www.medicalnewstoday.com --- 14 days ago
One out of every three Americans is obese. These individuals are at greater risk for additional diseases, since obesity leads to other health problems, such as diabetes. Obesity-related complications are associated with an abnormal fat metabolism in the muscle. As a result, accumulated fat by-products inside the muscle affect Insulin resistance. To avoid the build up of fat by-products, fat must either be oxidized (burned, as in exercise) or stored (as benign fat) in muscle. ...

Source: www.liebertonline.com --- 27 days ago
Rejuvenation Research Aug 2008, Vol. 11, No. 4: 725-733. Abstract Circulating Insulin-like growth factor-1 (IGF-1) levels are linked to cardiac performance and lifespan. However, the role of IGF-1 levels in aging-associated cardiac dysfunction has not been defined. This study was designed to evaluate the ... ...

Source: www.jci.org --- 36 days ago
Insulin resistance is a major metabolic feature of obesity and is a key factor in the etiology of a number of diseases, including type 2 diabetes. In this review, we discuss potential mechanisms by which brief nutrient excess and obesity lead to Insulin resistance and propose that these mechanisms of action are different but interrelated. We discuss how pathways that “sense” nutrients within skeletal muscle are readily able to regulate Insulin action. We then discuss how obesity leads to Insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. In particular, we focus on the hypothesis that the macrophage is an important cell type in the propagation of inflammation and induction of Insulin resistance in obesity. Overall, we provide our integrative perspective regarding how nutrients and obesity interact to regulate Insulin Sensitivity. ...

Source: www.ncbi.nlm.nih.gov --- 8 days ago
Related Articles Dark chocolate: consumption for pleasure or therapy? J Thromb Thrombolysis. 2008 Sep 23; Authors: Lippi G, Franchini M, Montagnana M, Favaloro EJ, Guidi GC, Targher G Traditional chocolate is derived from the cocoa bean, which is one of the most concentrated sources of flavanols, a subgroup of the natural antioxidant plant compounds called flavonoids. Accumulating evidence from the past 10 years demonstrates that moderate consumption of chocolate, especially dark chocolate, may exert protective effects against the development of cardiovascular disease. Several mechanisms have been proposed to explain this positive influence, including metabolic, antihypertensive, anti-inflammatory, and anti-thrombotic effects, as well as effects on Insulin Sensitivity and vascular endothelial function. Should these results be confirmed in randomised, controlled, cross-over, multi-dose trials, then the pleasure associated with chocolate consumption might also be justified from health and psychological perspectives. However, since dark chocolate has substantially higher levels of flavonoids than milk chocolate, and milk proteins may inhibit absorption of flavonoids, it might be preferable to consume dark chocolate than the white (milk) variety. PMID: 18827977 [PubMed - as supplied by publisher] ...

Source: www.ncbi.nlm.nih.gov --- 4 days ago
Related Articles Sex-related differences in the associations between hyperleptinemia, Insulin resistance and dysfibrinolysis. Blood Coagul Fibrinolysis. 2008 Oct;19(7):625-632 Authors: Eriksson MA, Rask E, Johnson O, Carlström K, Ahrén B, Eliasson M, Boman K, Söderberg S The adipocyte-derived hormone leptin is associated with Insulin resistance and reduced fibrinolytic status - or dysfibrinolysis - in humans. As leptin associates differentially to the development of cardiovascular disease and diabetes in men and women, we hypothesized that leptin and Insulin Sensitivity are related to dysfibrinolysis in a sex-dependent manner. Thirty-two men and 40 women were recruited from the Monitoring of trends and determinants in Cardiovascular disease (MONICA) population sample, representing the highest and lowest quartiles of fasting Insulin levels. Lipids, fibrinolytic status [plasminogen activator inhibitor 1 (PAI-1) activity, tissue plasminogen activator (tPA) mass and activity, and tPA-PAI complex], leptin, testosterone and sex-hormone-binding globulin were measured. Insulin Sensitivity was estimated using the euglycaemic clamp technique. Body composition was determined by bioimpedance. Determinants for circulating levels of fibrinolytic factors were explored in a multivariate linear regression analysis. Levels of fibrinolytic variables and estimated Insulin Sensitivity did not differ between men and women. Leptin was independently associate ...

Source: www.ncbi.nlm.nih.gov --- 6 days ago
Related Articles SHC-1/p52Shc targets the Insulin/IGF-1 and JNK signaling pathways to modulate life span and stress response in C. elegans. Genes Dev. 2008 Oct 1;22(19):2721-35 Authors: Neumann-Haefelin E, Qi W, Finkbeiner E, Walz G, Baumeister R, Hertweck M Correlative evidence links stress, accumulation of oxidative cellular damage, and aging in several species. Genetic studies in species ranging from yeast to mammals revealed several pathways regulating stress response and life span, including caloric intake, mitochondrial respiration, Insulin/IGF-1 (IIS), and JNK (c-Jun N-terminal kinase) signaling. How IIS and JNK signaling cross-talk to defend against diverse stressors contributing to aging is of critical importance but, so far, only poorly understood. In this study, we demonstrate that the adaptor protein SHC-1, the Caenorhabditis elegans homolog of human p52Shc, coordinates mechanisms of stress response and aging. Using genetic and biochemical approaches, we discover that SHC-1 not only opposes IIS but also activates JNK signaling. Loss of shc-1 function results in accelerated aging and enhanced Sensitivity to heat, oxidative stress, and heavy metals, whereas expression of human p52Shc rescues the shc-1 mutant phenotype. SHC-1 acts upstream of the Insulin/IGF receptor DAF-2 and the PI3 kinase AGE-1 and directly interacts with DAF-2. Moreover, SHC-1 activates JNK signaling by binding to MEK-1 kinase. Both aspects converge on co ...

Source: www.ncbi.nlm.nih.gov --- 1 day ago
Related Articles Lack of association of liver fat with model parameters of beta-cell function in men with impaired glucose tolerance and type 2 diabetes. Eur J Endocrinol. 2008 Sep;159(3):251-7 Authors: Tushuizen ME, Bunck MC, Pouwels PJ, Bontemps S, Mari A, Diamant M OBJECTIVE: Hepatic steatosis and obesity are components of the metabolic syndrome and risk factors for developing type 2 diabetes (T2DM). We studied how liver fat and body fat distribution relate to various aspects of beta-cell function. METHODS: In 12 men with T2DM, 10 men with impaired glucose tolerance (IGT), and 14 age- and body mass index-matched controls, we measured body fat distribution and liver fat by magnetic resonance imaging and spectroscopy. An oral glucose tolerance test was performed to calculate Insulin secretory rate (ISR) by C-peptide deconvolution, and beta-cell function using a mathematical model that describes ISR as a function of absolute glucose levels (Insulin secretory tone and glucose Sensitivity), the glucose rate of change (rate Sensitivity), and a potentiation factor. RESULTS: Waist circumference and the various body fat compartments did not differ among groups. IGT had the highest total and late phase Insulin secretion (P<0.001), whereas patients had the lowest insulinogenic index adjusted for Insulin resistance (P=0.006). In spite of the hypersecretion, IGT had beta-cell glucose Sensitivity, rate Sensitivity, and potentiation similar to con ...

Source: www.ncbi.nlm.nih.gov --- 1 day ago
Related Articles SirT1 gain of function increases energy efficiency and prevents diabetes in mice. Cell Metab. 2008 Oct;8(4):333-41 Authors: Banks AS, Kon N, Knight C, Matsumoto M, Gutiérrez-Juárez R, Rossetti L, Gu W, Accili D In yeast, worms, and flies, an extra copy of the gene encoding the Sirtuin Sir2 increases metabolic efficiency, as does administration of polyphenols like resveratrol, thought to act through Sirtuins. But evidence that Sirtuin gain of function results in increased metabolic efficiency in mammals is limited. We generated transgenic mice with moderate overexpression of SirT1, designed to mimic the Sirtuin gain of function that improves metabolism in C. elegans. These mice exhibit normal Insulin Sensitivity but decreased food intake and locomotor activity, resulting in decreased energy expenditure. However, in various models of Insulin resistance and diabetes, SirT1 transgenics display improved glucose tolerance due to decreased hepatic glucose production and increased adiponectin levels, without changes in body weight or composition. We conclude that SirT1 gain of function primes the organism for metabolic adaptation to Insulin resistance, increasing hepatic Insulin Sensitivity and decreasing whole-body energy requirements. These findings have important implications for Sirtuin-based therapies in humans. PMID: 18840364 [PubMed - in process] ...

Source: www.ncbi.nlm.nih.gov --- 7 days ago
Related Articles Phenotypic switching of adipose tissue macrophages with obesity is generated by spatiotemporal differences in macrophage subtypes. Diabetes. 2008 Oct 1; Authors: Lumeng CN, Delproposto JB, Westcott DJ, Saltiel AR Objective: To establish the mechanism of the phenotypic switch of adipose tissue macrophages from an alternatively activated (M2a) to a classically activated (M1) phenotype with obesity. Research Design and Methods: ATMs from lean and obese (high fat diet fed) C57Bl/6 mice were analyzed by a combination of flow cytometry, immunofluorescence, and expression analysis for M2a and M1 genes. Pulse labeling of ATMs with PKH26 assessed the recruitment rate of ATMs to spatially distinct regions. Results: Resident ATMs in lean mice express the M2a marker MGL1 and localize to interstitial spaces between adipocytes independent of CCR2 and CCL2. With diet-induced obesity, MGL1(+) ATMs remain in interstitial spaces, while a population of MGL1(-)CCR2(+) ATMs with high M1 and low M2a gene expression is recruited to clusters surrounding necrotic adipocytes. Pulse labeling showed that the rate of recruitment of new macrophages to MGL1(-) ATM clusters is significantly faster than that of interstitial MGL1(+) ATMs. This recruitment is attenuated in Ccr2(-/-) mice. M2a and M1 polarized macrophages produced different effects on adipogenesis and adipocyte Insulin Sensitivity in vitro. Conclusions: The shift in the M2a/M1 ATM balan ...

Source: www.ncbi.nlm.nih.gov --- 38 days ago
Related Articles The estrogen receptor alpha-selective agonist PPT improves glucose tolerance in ob/ob mice; potential molecular mechanisms. J Endocrinol. 2008 Aug 29; Authors: Lundholm L, Bryzgalova G, Gao H, Portwood N, Fält S, Berndt K, Dicker A, Galuska D, Zierath J, Gustafsson JA, Efendic S, Dahlman-Wright K, Khan A The aim of this study was to validate the role of estrogen receptor alpha (ERalpha) signaling in the regulation of glucose metabolism, and to compare the molecular events upon treatment with the estrogen receptor alpha-selective agonist propyl pyrazole triol (PPT) or estradiol (E2) in ob/ob mice. Female ob/ob mice were treated with PPT, E2 or vehicle for 7 or 30 days. Intraperitoneal glucose and Insulin tolerance tests were performed, and Insulin secretion was determined from isolated islets. Glucose uptake was assayed in isolated skeletal muscle and adipocytes. Gene expression profiling in the liver was performed using Affymetrix microarrays, and the expression of selected genes was studied by real-time PCR analysis. PPT and E2 treatment improved glucose tolerance and Insulin Sensitivity. Fasting blood glucose levels were decreased after 30 days of PPT and E2 treatment. Additionally, PPT and E2 decreased basal Insulin levels and improved the acute Insulin response, with no effect on Insulin secretion from isolated islets. Basal and Insulin-stimulated glucose uptake in skeletal muscle and adipose tissue were similar be ...

Source: www.ncbi.nlm.nih.gov --- 10 days ago
Related Articles Adiponectin Multimers and Metabolic Syndrome Traits: Relative Adiponectin Resistance in African Americans. Obesity (Silver Spring). 2008 Sep 25; Authors: Lara-Castro C, Doud EC, Tapia PC, Munoz AJ, Fernandez JR, Hunter GR, Gower BA, Garvey WT African Americans (AAs) tend to have lower total adiponectin levels compared to European Americans (EA); however, it is not known whether race affects adiponectin multimer distribution and their relationships to metabolic traits. We measured total adiponectin, high molecular weight (HMW), low molecular weight (LMW) (i.e., hexamer), and trimer adiponectin in 132 normoglycemic premenopausal women (75 AAs, 57 EAs), together with measures of total and abdominal fat, plasma lipids, Insulin Sensitivity (S(i)), and genetic admixture estimates. We found that lower total adiponectin in AAs was explained by reduced LMW, and trimer forms because levels of HMW did not differ between races. In EAs, HMW was highly correlated with multiple metabolic syndrome traits. In contrast, the LMW and trimer forms were most highly correlated with metabolic traits in AAs, including abdominal adiposity, lipids, and S(i). At similar levels of visceral adiposity, AAs exhibited significantly lower LMW adiponectin than EAs. Similarly, at comparable levels of HMW and LMW adiponectin, AAs were more Insulin resistant than their EA counterparts. In conclusion, (i) serum adiponectin is lower in AAs predominantly as ...

Source: www.ncbi.nlm.nih.gov --- 24 days ago
Related Articles Nonalcoholic fatty liver disease is associated with hepatic and skeletal muscle Insulin resistance in overweight adolescents. Am J Clin Nutr. 2008 Aug;88(2):257-62 Authors: Deivanayagam S, Mohammed BS, Vitola BE, Naguib GH, Keshen TH, Kirk EP, Klein S BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) and Insulin resistance are common in overweight adolescents. OBJECTIVE: The purpose of this study was to determine the relation between NAFLD and Insulin Sensitivity in liver and skeletal muscle by studying overweight adolescents with a normal or high intrahepatic triglyceride (IHTG) content, who were matched for age, sex, body mass index (BMI; in kg/m(2)), and Tanner stage. DESIGN: Stable-isotope-labeled tracer infusion and the hyperinsulinemic-euglycemic clamp procedure were used to assess skeletal muscle and hepatic Insulin Sensitivity, and magnetic resonance spectroscopy was used to assess the IHTG content in 10 overweight (BMI = 35.9 +/- 1.3) adolescents with NAFLD (IHTG = 28.4 +/- 3.4%) and 10 overweight (BMI = 36.6 +/- 1.5) adolescents with a normal IHTG content (3.3 +/- 0.5%). RESULTS: The baseline plasma glucose concentration and the rate of appearance of glucose in plasma were the same in subjects with a normal (87.1 +/- 1.2 mg/dL, 16.2 +/- 1.1 micromol . kg fat-free mass(-1) . min(-1)) or high (89.2 +/- 2.5 mg/dL, 16.3 +/- 1.2 micromol . kg fat-free mass(-1) . min(-1)) IHTG content. However, compared with sub ...

Source: www.ncbi.nlm.nih.gov --- 12 days ago
Inhibition of CCR2 Ameliorates Insulin Resistance and Hepatic Steatosis in db/db Mice. Arterioscler Thromb Vasc Biol. 2008 Sep 25; Authors: Tamura Y, Sugimoto M, Murayama T, Ueda Y, Kanamori H, Ono K, Ariyasu H, Akamizu T, Kita T, Yokode M, Arai H OBJECTIVE: Recently, adipose tissue inflammation induced by macrophage infiltration through MCP-1/C-C chemokine receptor-2 (CCR2) pathway is considered to play a role in the development of visceral obesity and Insulin resistance. In the present study, to further examine the role of CCR2 in the development of obesity and type 2 diabetes, we studied the effect of pharmacological inhibition of CCR2 from the early stage of obesity in db/db mice. METHODS AND RESULTS: Db/+m (lean control) and db/db mice were fed with a standard diet with or without 0.005% propagermanium, as a CCR2 inhibitor for 12 weeks from 6 weeks of age. Propagermanium treatment decreased body weight gain, visceral fat accumulation, and the size of adipocytes only in db/db mice. Further, propagermanium suppressed macrophage accumulation and inflammation in adipose tissue. Propagermanium treatment also ameliorated glucose tolerance and Insulin Sensitivity, and decreased hepatic triglyceride contents in db/db mice. CONCLUSIONS: Propagermanium improved obesity and related metabolic disorders, such as Insulin resistance and hepatic steatosis by suppressing inflammation in adipose tissue. Our data indicate that inhibition of CCR2 co ...

Source: www.moreover.com --- 10 days ago
The findings indicate even one bout of exercise helps to reduce the fat by-products inside the muscle, which affects Insulin Sensitivity. ...

Source: www.ncbi.nlm.nih.gov --- 12 days ago
Related Articles Food restriction and streptozotocin treatment decrease 5-HT1A and 5-HT2A receptor-mediated behavioral effects in rats. Behav Pharmacol. 2008 Jul;19(4):292-7 Authors: Li JX, France CP Food restriction and hypoinsulinemia can affect the synthesis, turnover, and receptor function of serotonin (5-HT) in brain. This study explored the effects of food restriction and streptozotocin treatment on behavioral effects related to 5-HT1A (+)-8-hydroxy-2-(dipropylamino)tetralin hydrobromide (8-OH-DPAT) and 5-HT2A [(+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI)] receptor activation. Lower lip retraction and flat body posture (8-OH-DPAT) and head twitching (DOI) were measured in rats during free feeding, food restriction, after treatment with streptozotocin, and finally after Insulin replacement. 8-OH-DPAT induced lower lip retraction and flat body posture whereas DOI induced head twitching. One week of food restriction (10 g/day) decreased 8-OH-DPAT-induced lower lip retraction, 8-OH-DPAT-induced flat body posture, and DOI-induced head twitching. Subsequently, 1 week of free access to food restored Sensitivity to 8-OH-DPAT and DOI-induced behavioral effects. Finally, 1 week after streptozotocin, 8-OH-DPAT-induced flat body posture and DOI-induced head twitching were markedly reduced whereas 8-OH-DPAT-induced lower lip retraction was unchanged. One week of Insulin replacement restored Sensitivity to 8-OH-DPAT and DOI-induce ...

Source: www.ncbi.nlm.nih.gov --- 14 days ago
Related Articles Activation of hypothalamic S6 kinase mediates diet-induced hepatic Insulin resistance in rats. J Clin Invest. 2008 Aug;118(8):2959-68 Authors: Ono H, Pocai A, Wang Y, Sakoda H, Asano T, Backer JM, Schwartz GJ, Rossetti L Prolonged activation of p70 S6 kinase (S6K) by Insulin and nutrients leads to inhibition of Insulin signaling via negative feedback input to the signaling factor IRS-1. Systemic deletion of S6K protects against diet-induced obesity and enhances Insulin Sensitivity in mice. Herein, we present evidence suggesting that hypothalamic S6K activation is involved in the pathogenesis of diet-induced hepatic Insulin resistance. Extending previous findings that Insulin suppresses hepatic glucose production (HGP) partly via its effect in the hypothalamus, we report that this effect was blunted by short-term high-fat diet (HFD) feeding, with concomitant suppression of Insulin signaling and activation of S6K in the mediobasal hypothalamus (MBH). Constitutive activation of S6K in the MBH mimicked the effect of the HFD in normal chow-fed animals, while suppression of S6K by overexpression of dominant-negative S6K or dominant-negative raptor in the MBH restored the ability of MBH Insulin to suppress HGP after HFD feeding. These results suggest that activation of hypothalamic S6K contributes to hepatic Insulin resistance in response to short-term nutrient excess. PMID: 18618016 [PubMed - indexed for MEDLINE] ...

Source: www.ncbi.nlm.nih.gov --- 37 days ago
Related Articles Sleep-disordered breathing in children with metabolic syndrome: the role of leptin and sympathetic nervous system activity and the effect of continuous positive airway pressure. Pediatrics. 2008 Sep;122(3):e634-42 Authors: Nakra N, Bhargava S, Dzuira J, Caprio S, Bazzy-Asaad A OBJECTIVE. The purpose of this work was to determine whether, in children with metabolic syndrome and sleep-disordered breathing, metabolic markers separate them from children with metabolic syndrome without sleep-disordered breathing and whether treatment of sleep-disordered breathing with continuous positive airway pressure is associated with an improvement in metabolic derangement. PATIENTS AND METHODS. Subjects aged 7 to 19 years old with metabolic syndrome and a positive validated sleep questionnaire were recruited. Subjects underwent overnight polysomnography, during which sympathetic nervous system activity was assessed via 8-hourly measurements of norepinephrine and epinephrine, together with leptin. The next morning, a fasting 3-hour oral glucose-tolerance test was performed to calculate whole-body Insulin Sensitivity. A fasting lipid panel interleukin 6, adiponectin, and C-reactive protein levels were also measured. Children with sleep-disordered breathing were placed on continuous positive airway pressure for 3 months and studied again. Sleep-disordered breathing and no sleep-disordered breathing groups were compared by using Fisher's ...