scholarly journals Circulating Prokineticin 2 Levels Are Increased in Children with Obesity and Correlated with Insulin Resistance

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Han Wang ◽  
Yanjun Jia ◽  
Xiaoyan Yu ◽  
Li Peng ◽  
Chunfeng Mou ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Binary Logistic Regression ◽  
Normal Weight ◽  
Gamma Glutamyl Transpeptidase ◽  
Nonalcoholic Fatty Liver ◽  
Prokineticin 2 ◽  
Biochemical Measurements ◽  
Regulate Food Intake

Objective. Prokineticin 2 (PK2) has been shown to regulate food intake, fat production, and the inflammation process, which play vital roles in the pathogenesis of obesity. The first aim of this study was to investigate serum PK2 levels in children with obesity and normal-weight children. The second aim was to compare the levels of PK2 between children with obesity, with and without nonalcoholic fatty liver disease (NAFLD). Methods. Seventy normal-weight children and 91 children with obesity (22 with NAFLD) were recruited. Circulating PK2, IL-6, and TNF-α were measured by enzyme-linked immunosorbent assays. Anthropometric and biochemical measurements related to adiposity, lipid profile, and insulin resistance were examined for all participants. Results. Serum PK2 was significantly higher in children with obesity than in the normal-weight controls. Circulating PK2 levels were not different between the patients with and without NAFLD. Circulating PK2 was positively correlated with BMI, BMI z-score, insulin, glucose, HOMA-IR, total cholesterol, low-density lipoprotein cholesterol, alanine aminotransferase, and gamma-glutamyl transpeptidase. Binary logistic regression revealed that the odds ratios for obesity were significantly elevated with increasing PK2. Conclusions. PK2 was strongly associated with obesity, and it may also be related to metabolic disorders and insulin resistance. This trial is registered with ChiCTR2000038838.

Pathophysiology of type 2 diabetes mellitus

2011 ◽  
pp. 1740-1748 ◽  
Author(s):  
Hannele Yki-Järvinen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Glucagon Secretion ◽  
Normal Subjects ◽  
Nonalcoholic Fatty Liver ◽  
Insulin And Glucagon Secretion

Insulin resistance, largely caused by obesity and physical inactivity, both precedes and predicts type 2 diabetes. The insulin resistance preceding type 2 diabetes is commonly referred to as the metabolic syndrome. The latter condition consists of a cluster of risk factors, which are thought to be either causes or consequences of insulin resistance. The development of type 2 diabetes, overt hyperglycaemia, also requires the presence of a relative defect in insulin secretion. This defect appears, at least in part, genetically determined. Insulin resistance can be defined as the inability of insulin to produce its usual biological actions at circulating concentrations that are effective in normal subjects. This chapter is focused on defining and characterizing defects in insulin action and in insulin and glucagon secretion in patients with type 2 diabetes, and the effects that these defects have on the body. The causes of insulin resistance in different tissues is also discussed. Hepatic insulin resistance and metabolic syndrome can be linked to atherosclerosis and cardiovascular disease, the main cause of the excess mortality in type 2 diabetes, by increased very-low-density lipoprotein production which leads to the generation of small, dense, and atherogenic LDL particles. Insulin resistance is also seen in adipose tissue and skeletal muscle, altering glucose and fatty acid handling in these tissues and the liver. The hepatic manifestation of insulin resistance in type 2 diabetes is nonalcoholic fatty liver disease (NAFLD). NFALD is defined as excess fat in the liver which is not due to excess alcohol use, and can lead to hepatic inflammation and even cirrhosis. There are defects in both insulin and glucagon secretion in type 2 diabetes, the exact cause of which remains speculative. Whilst family history and genetic factors appear to play a significant role in determining the susceptibility to overt type 2 diabetes, the only certain aspect of its aetiology and pathogenesis is that its incidence can very significantly be reduced by increasing physical activity and avoiding obesity.

scholarly journals Scutellaria baicalensis Alleviates Insulin Resistance in Diet-Induced Obese Mice by Modulating Inflammation

2019 ◽  
Vol 20 (3) ◽  
pp. 727 ◽  
Author(s):  
Hyun-Young Na ◽  
Byung-Cheol Lee
Keyword(s):  
Insulin Resistance ◽  
Inflammatory Responses ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Postprandial Glucose ◽  
Scutellaria Baicalensis ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Epididymal Fat

Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.

Low density lipoprotein particle size and risk factors of insulin resistance syndrome

2000 ◽  
Vol 148 (1) ◽  
pp. 141-149 ◽  
Author(s):  
Yechiel Friedlander ◽  
Miriam Kidron ◽  
Muriel Caslake ◽  
Tracey Lamb ◽  
Michael McConnell ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Particle Size ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Insulin Resistance Syndrome ◽  
Low Density ◽  
Lipoprotein Particle ◽  
Lipoprotein Particle Size

scholarly journals Macrophage LRP1 Promotes Diet-Induced Hepatic Inflammation and Metabolic Dysfunction by Modulating Wnt Signaling

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Dianaly T. Au ◽  
Mary Migliorini ◽  
Dudley K. Strickland ◽  
Selen C. Muratoglu
Keyword(s):  
Insulin Resistance ◽  
Wnt Signaling ◽  
Cholesterol Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Hepatic Inflammation ◽  
Low Density Lipoprotein Receptor ◽  
Density Lipoprotein Receptor

Hepatic inflammation is associated with the development of insulin resistance, which can perpetuate the disease state and may increase the risk of metabolic syndrome and diabetes. Despite recent advances, mechanisms linking hepatic inflammation and insulin resistance are still unclear. The low-density lipoprotein receptor-related protein 1 (LRP1) is a large endocytic and signaling receptor that is highly expressed in macrophages, adipocytes, hepatocytes, and vascular smooth muscle cells. To investigate the potential role of macrophage LRP1 in hepatic inflammation and insulin resistance, we conducted experiments using macrophage-specific LRP1-deficient mice (macLRP1−/−) generated on a low-density lipoprotein receptor knockout (LDLR−/−) background and fed a Western diet. LDLR−/−; macLRP1−/− mice gained less body weight and had improved glucose tolerance compared to LDLR−/− mice. Livers from LDLR−/−; macLRP1−/− mice displayed lower levels of gene expression for several inflammatory cytokines, including Ccl3, Ccl4, Ccl8, Ccr1, Ccr2, Cxcl9, and Tnf, and reduced phosphorylation of GSK3α and p38 MAPK proteins. Furthermore, LRP1-deficient peritoneal macrophages displayed altered cholesterol metabolism. Finally, circulating levels of sFRP-5, a potent anti-inflammatory adipokine that functions as a decoy receptor for Wnt5a, were elevated in LDLR−/−; macLRP1−/− mice. Surface plasmon resonance experiments revealed that sFRP-5 is a novel high affinity ligand for LRP1, revealing that LRP1 regulates levels of this inhibitor of Wnt5a-mediated signaling. Collectively, our results suggest that LRP1 expression in macrophages promotes hepatic inflammation and the development of glucose intolerance and insulin resistance by modulating Wnt signaling.

scholarly journals Biological Pathways in Adolescent Aortic Stiffness

2021 ◽  
Vol 10 (6) ◽  
Author(s):  
Justin P. Zachariah ◽  
Yunfei Wang ◽  
Jane W. Newburger ◽  
Sarah D. deFerranti ◽  
Gary F Mitchell ◽  
...  
Keyword(s):  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Aortic Stiffness ◽  
Pulse Wave ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Normal Weight ◽  
Excess Weight ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol

Background Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflammation, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we assessed the relations of comprehensive measures of aortic stiffness with body mass index (BMI) and related but distinct circulating biomarkers. Methods and Results A convenience sample of 246 adolescents (mean age, 16±2 years; 45% female, 24% Black, and 43% Hispanic) attending primary care or preventive cardiology clinics at 2 tertiary hospitals was grouped as normal weight (N=98) or excess weight (N=148, defined as BMI ≥age‐ and sex‐referenced 85th percentile). After an overnight fast, participants underwent anthropometry, noninvasive arterial tonometry, and assays for serum lipids, CRP (C‐reactive protein), glucose, insulin, renin, aldosterone, and leptin. We used multivariable linear regression to relate arterial stiffness markers (including carotid‐femoral pulse wave velocity) to BMI z score and a biomarker panel. Carotid‐femoral pulse wave velocity was higher in excess weight compared with normal weight group (5.0±0.7 versus 4.6±0.6 m/s; P <0.01). After multivariable adjustment, carotid‐femoral pulse wave velocity was associated with BMI z score (0.09 [95% CI, 0.01–0.18]; P =0.04) and with low‐density lipoprotein cholesterol (0.26 [95% CI, 0.03–0.50]; P =0.03). Conclusions Higher BMI and low‐density lipoprotein cholesterol were associated with greater aortic stiffness in adolescents. Maintaining optimal BMI and lipid levels may mitigate aortic stiffness.

scholarly journals Pro-atherogenic lipid profile in pulmonary tuberculosis patients with concurrent insulin resistance

2021 ◽  
Vol 8 (2) ◽  
pp. 111-114
Author(s):  
Olga Shvets ◽  
Olga Shevchenko ◽  
Zoriana Piskur ◽  
Hanna Stepanenko ◽  
Olha Pohorielova
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Pulmonary Tuberculosis ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Tuberculosis Patients ◽  
Group 2 ◽  
Group 1

Background. The problem of studying lipid metabolism in patients with tuberculosis is of interest to scientists around the world. The purpose of the study - to investigate lipid profile in pulmonary tuberculosis patients with concurrent insulin resistance. Materials and methods. Forty-one patients with pulmonary tuberculosis were examined. Insulin resistance index (HOMA-IR), total cholesterol level (TC), triglycerides (TG) level, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and atherogenic index (AI) were measured. Results. Group 1 - 26 patients with tuberculosis and insulin resistance (HOMA-IR ˃ 2.7); Group 2 – 15 patients with tuberculosis without insulin resistance (HOMA-IR ˂ 2.7). Group 1 patients had severe course of TB with fever, severe fatigue and weakness, profuse sweating, weight loss, cough and shortness of breath. Median TC indices differed at significant level (p = 0.012): group 1 - 4.82 mmol/l, group 2 - 4.25 mmol/l. TG level was higher in group 1 patients - 1.32 mmol/l than in group 2 patients - 1.28 mmol/l. LDL cholesterol values were higher in group 1 patients - 3.2 mmol/l vs 2.5 mmol/l in group 2. The AI was higher in group1 (p = 0.005): 3.9 units against 2.8 units in group 2 patients. Conclusions. Insulin resistance in pulmonary tuberculosis patients was associated with severe course of the disease, severe clinical manifestations and impaired external respiration. Pro-atherogenic disorders of lipid metabolism in pulmonary tuberculosis patients with concurrent insulin resistance can be considered as the degree of endogenous intoxication.

scholarly journals VARIANTS OF HYPERLIPIDEMIA IN CHILDREN WITH INSULIN RESISTANCE

2020 ◽  
Vol 7 (1) ◽  
pp. 23-25
Author(s):  
T. Chaychenko ◽  
M. Kharkova ◽  
O. Rybka
Keyword(s):  
Insulin Resistance ◽  
Lipid Profile ◽  
National Cholesterol Education Program ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Overweight Children ◽  
Obese Children ◽  
Age Assessment ◽  
Gender And Age ◽  
Adults And Children

Obesity in adults and children is characterized by epidemiological prevalence with a tendency to increase. Purpose of the study- to analyze the lipid profile in overweight children, depending on the presence of insulin resistance. 247 overweight and obese children aged 2 to 18 were examined, including 160 boys and 87 girls. Obesity was diagnosed if the BMI exceeded 97 percentile, according to gender and age. Assessment of the lipid profile included measurements of total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein. To evaluate the parameters of the lipid profile, we used the National Cholesterol Education Program (NCEP) according to the latest edition (2006). We analyzed lipid values depending on the presence or absence of insulin resistance. BMI was also evaluated according to Z-BMI. Insulin resistance was detected in 69.9% of children. Hyperlipidemia was detected in 24.9% of children and dyslipidemia in 83% of the children examined. A change was found in all indicators of the lipid profile, depending on the presence of insulin resistance. A significant increase in Z-BMI was revealed depending on the presence of insulin resistance. Conclusions: Most overweight children have insulin resistance and dyslipidemia; the type of dyslipidemia in children with obesity directly depends on the presence of insulin resistance.

Abstract P080: Fructose Acutely Increases Size of Very Low Density Lipoprotein In Adolescents With Hepatic Steatosis

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Mirian Vos ◽  
Ran Jin ◽  
Jean Welsh ◽  
Ngoc-Anh Le
Keyword(s):  
Hepatic Steatosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cardiovascular Complications ◽  
Plasma Lipoproteins ◽  
Healthy Children ◽  
Mri Imaging ◽  
Nonalcoholic Fatty Liver ◽  
Obese Adolescents ◽  
Acute Response

Introduction: Cardiovascular complications are a leading cause of mortality in nonalcoholic fatty liver disease (NAFLD). Fructose has been reported to be associated with dyslipidemia and increased cardiovascular risk in adults but its impact on adolescents with NAFLD is not well understood. We previously demonstrated that fructose disproportionately increased postprandial hypertriglyceridemia in pediatric NAFLD as compared to healthy children. However, the mechanism remains unclear. Hypothesis: We hypothesized that fructose would contribute to hypertriglyceridemia in pediatric NAFLD by increasing the size of VLDL particles. Methods: We examined the acute response to a single dose of fructose beverage in 50 Hispanic-American obese adolescents with varying degrees of hepatic steatosis. Those with hepatic fat >5% on MRI imaging were designated as presumed NAFLD. Subjects consumed a 12oz drink containing 33g of fructose and plasma samples were collected at baseline and 30, 60, and 90 minutes afterwards. Plasma lipoproteins were measured using NMR (Liposcience, Raleigh, NC). Results: In response to acute fructose load, subjects without NAFLD increased the total number of TG rich lipoprotein particles (p = 0.047). However, this increase was not observed in subjects with NAFLD; instead, they increased the subpopulation of large VLDL particles (p = 0.008) and the mean size of VLDL particles (p = 0.004) (Figure 1). In line with this finding, TG-to-apoB ratio significantly increased in subjects with NAFLD (2.25 ± 0.26 to 2.37 ± 0.25, p = 0.031) but not in non-NAFLD. Conclusions: These findings demonstrate that adolescents with NAFLD have more atherogenic, large VLDL in response to fructose compared to obese adolescents without NAFLD. Dietary fructose restriction may be a critical component in the treatment of NAFLD associated cardiovascular disease and should be tested further.

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