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How Abdominal Fibrogenesis Affects Adolescents With Obesity
TOPLINE:
Insulin resistance and obesity in adolescents may lead to increased abdominal fibrogenesis, impairing the capacity of the abdominal subcutaneous adipose tissue (SAT) to store lipids, which may cause fat accumulation in the visceral adipose tissue (VAT) depot and in other organs such as the liver.
METHODOLOGY:
- Abdominal fibrogenesis, but not adipose tissue expandability, is known to increase in adults with obesity and reduce insulin sensitivity; however, little is known about fibrogenesis in adolescents with obesity.
- In this study, researchers investigated if lipid dynamics, fibrogenesis, and abdominal and gluteal adipocyte turnover show dysregulation to a greater extent in insulin-resistant adolescents with obesity than in insulin-sensitive adolescents with obesity.
- They recruited 14 individuals between 12 and 20 years with a body mass index over 30 from the Yale Clinic, of whom seven participants were classified as insulin resistant.
- Deuterated water methodologies were used to study the indices of adipocyte turnover, lipid dynamics, and fibrogenesis in abdominal and gluteal fat deposits.
- A 3-hour oral glucose tolerance test and multisection MRI scan of the abdominal region were used to assess the indices of glucose metabolism, abdominal fat distribution patterns, and liver fat content.
TAKEAWAY:
- The abdominal and gluteal SAT turnover rate of lipid components (triglyceride production and breakdown as well as de novo lipogenesis contribution) was similar in insulin-resistant and insulin-sensitive adolescents with obesity.
- The insoluble collagen (type I, subunit alpha2) level was higher in the abdominal adipose tissue of insulin-resistant adolescents than in insulin-sensitive adolescents (difference in fractional synthesis rate, 0.611; P < .001), indicating increased abdominal fibrogenesis.
- Abdominal insoluble collagen I alpha2 was associated with higher fasting plasma insulin levels (correlation [r], 0.579; P = .015), a higher visceral to total adipose tissue ratio (r, 0.643; P = .007), and a lower whole-body insulin sensitivity index (r, -0.540; P = .023).
- There was no evidence of increased collagen production in the gluteal adipose tissue, and as a result, fibrogenesis was observed.
IN PRACTICE:
“The increased formation of insoluble collagen observed in insulin-resistant compared with insulin-sensitive individuals contributes to lipid spillover from SAT to VAT and, in turn, serves as a critically important mechanism involved in the complex sequelae of obesity-related metabolic and liver disease pathology,” the authors wrote.
SOURCE:
This study, led by Aaron L. Slusher, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, was published online in Obesity.
LIMITATIONS:
The researchers did not measure hepatic collagen synthesis rates. The analysis was performed on a small study population. The authors were also unable to assess potential sex differences.
DISCLOSURES:
The study was funded by the Foundation for the National Institutes of Health and Clara Guthrie Patterson Trust Mentored Research Award. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Insulin resistance and obesity in adolescents may lead to increased abdominal fibrogenesis, impairing the capacity of the abdominal subcutaneous adipose tissue (SAT) to store lipids, which may cause fat accumulation in the visceral adipose tissue (VAT) depot and in other organs such as the liver.
METHODOLOGY:
- Abdominal fibrogenesis, but not adipose tissue expandability, is known to increase in adults with obesity and reduce insulin sensitivity; however, little is known about fibrogenesis in adolescents with obesity.
- In this study, researchers investigated if lipid dynamics, fibrogenesis, and abdominal and gluteal adipocyte turnover show dysregulation to a greater extent in insulin-resistant adolescents with obesity than in insulin-sensitive adolescents with obesity.
- They recruited 14 individuals between 12 and 20 years with a body mass index over 30 from the Yale Clinic, of whom seven participants were classified as insulin resistant.
- Deuterated water methodologies were used to study the indices of adipocyte turnover, lipid dynamics, and fibrogenesis in abdominal and gluteal fat deposits.
- A 3-hour oral glucose tolerance test and multisection MRI scan of the abdominal region were used to assess the indices of glucose metabolism, abdominal fat distribution patterns, and liver fat content.
TAKEAWAY:
- The abdominal and gluteal SAT turnover rate of lipid components (triglyceride production and breakdown as well as de novo lipogenesis contribution) was similar in insulin-resistant and insulin-sensitive adolescents with obesity.
- The insoluble collagen (type I, subunit alpha2) level was higher in the abdominal adipose tissue of insulin-resistant adolescents than in insulin-sensitive adolescents (difference in fractional synthesis rate, 0.611; P < .001), indicating increased abdominal fibrogenesis.
- Abdominal insoluble collagen I alpha2 was associated with higher fasting plasma insulin levels (correlation [r], 0.579; P = .015), a higher visceral to total adipose tissue ratio (r, 0.643; P = .007), and a lower whole-body insulin sensitivity index (r, -0.540; P = .023).
- There was no evidence of increased collagen production in the gluteal adipose tissue, and as a result, fibrogenesis was observed.
IN PRACTICE:
“The increased formation of insoluble collagen observed in insulin-resistant compared with insulin-sensitive individuals contributes to lipid spillover from SAT to VAT and, in turn, serves as a critically important mechanism involved in the complex sequelae of obesity-related metabolic and liver disease pathology,” the authors wrote.
SOURCE:
This study, led by Aaron L. Slusher, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, was published online in Obesity.
LIMITATIONS:
The researchers did not measure hepatic collagen synthesis rates. The analysis was performed on a small study population. The authors were also unable to assess potential sex differences.
DISCLOSURES:
The study was funded by the Foundation for the National Institutes of Health and Clara Guthrie Patterson Trust Mentored Research Award. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Insulin resistance and obesity in adolescents may lead to increased abdominal fibrogenesis, impairing the capacity of the abdominal subcutaneous adipose tissue (SAT) to store lipids, which may cause fat accumulation in the visceral adipose tissue (VAT) depot and in other organs such as the liver.
METHODOLOGY:
- Abdominal fibrogenesis, but not adipose tissue expandability, is known to increase in adults with obesity and reduce insulin sensitivity; however, little is known about fibrogenesis in adolescents with obesity.
- In this study, researchers investigated if lipid dynamics, fibrogenesis, and abdominal and gluteal adipocyte turnover show dysregulation to a greater extent in insulin-resistant adolescents with obesity than in insulin-sensitive adolescents with obesity.
- They recruited 14 individuals between 12 and 20 years with a body mass index over 30 from the Yale Clinic, of whom seven participants were classified as insulin resistant.
- Deuterated water methodologies were used to study the indices of adipocyte turnover, lipid dynamics, and fibrogenesis in abdominal and gluteal fat deposits.
- A 3-hour oral glucose tolerance test and multisection MRI scan of the abdominal region were used to assess the indices of glucose metabolism, abdominal fat distribution patterns, and liver fat content.
TAKEAWAY:
- The abdominal and gluteal SAT turnover rate of lipid components (triglyceride production and breakdown as well as de novo lipogenesis contribution) was similar in insulin-resistant and insulin-sensitive adolescents with obesity.
- The insoluble collagen (type I, subunit alpha2) level was higher in the abdominal adipose tissue of insulin-resistant adolescents than in insulin-sensitive adolescents (difference in fractional synthesis rate, 0.611; P < .001), indicating increased abdominal fibrogenesis.
- Abdominal insoluble collagen I alpha2 was associated with higher fasting plasma insulin levels (correlation [r], 0.579; P = .015), a higher visceral to total adipose tissue ratio (r, 0.643; P = .007), and a lower whole-body insulin sensitivity index (r, -0.540; P = .023).
- There was no evidence of increased collagen production in the gluteal adipose tissue, and as a result, fibrogenesis was observed.
IN PRACTICE:
“The increased formation of insoluble collagen observed in insulin-resistant compared with insulin-sensitive individuals contributes to lipid spillover from SAT to VAT and, in turn, serves as a critically important mechanism involved in the complex sequelae of obesity-related metabolic and liver disease pathology,” the authors wrote.
SOURCE:
This study, led by Aaron L. Slusher, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, was published online in Obesity.
LIMITATIONS:
The researchers did not measure hepatic collagen synthesis rates. The analysis was performed on a small study population. The authors were also unable to assess potential sex differences.
DISCLOSURES:
The study was funded by the Foundation for the National Institutes of Health and Clara Guthrie Patterson Trust Mentored Research Award. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
Tuberculosis Screening Gaps Persist in New DMARD Users
TOPLINE:
The rates of screening for latent tuberculosis remain suboptimal among new users of biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), with notable variations by medication type and demographic characteristics.
METHODOLOGY:
- Professional society guidelines recommend screening for tuberculosis before starting treatment with most b/tsDMARDs.
- In an attempt to estimate the extent of latent tuberculosis screening, researchers combined claims and electronic health record datasets to evaluate 2853 new b/tsDMARD users (mean age, 73 years; 72% women; and 73% non-Hispanic White).
- The primary analysis focused on assessing the proportion of patients screened for latent tuberculosis in the year before starting a new b/tsDMARD.
- A sensitivity analysis evaluated the extent of screening within the 3 years preceding the initiation of a new b/tsDMARD.
- A total of 65.6% of patients received screening for latent tuberculosis in the year before initiating a new b/tsDMARD.
- Screening rates improved only slightly on expanding the window to 3 years, with 72.9% of patients receiving any tuberculosis screening.
- When stratified by drug type, over half of new users of Janus kinase inhibitors and nearly 90% of new users of interleukin-17 inhibitors had not received screening.
- Hispanic patients had lower odds of tuberculosis screening within 1 year than White patients (odds ratio [OR], 0.64; 95% CI, 0.46-0.90), as did those in the highest socioeconomic quartile, compared with the lowest (OR, 0.61; 95% CI, 0.40-0.94).
IN PRACTICE:
“Educational initiatives, team-based care delivery, task shifting, and technological interventions to address observed gaps in patient safety procedures are needed,” the authors wrote.
SOURCE:
The study was led by Eric T. Roberts, PhD, University of California, San Francisco, and published online in Arthritis Care & Research
LIMITATIONS:
The study lacked access to scanned documents or clinical notes, which may have resulted in the omission of a small number of tests that had no Medicare billing. Moreover, the study was restricted to a 3-year lookback period, potentially missing some remote screenings. The findings may have limited generalizability to younger patients or those not dually eligible for Medicare and Medicaid.
DISCLOSURES:
This study was funded by grants from the Agency for Healthcare Research and Quality and the National Institute for Arthritis and Musculoskeletal and Skin Diseases. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
The rates of screening for latent tuberculosis remain suboptimal among new users of biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), with notable variations by medication type and demographic characteristics.
METHODOLOGY:
- Professional society guidelines recommend screening for tuberculosis before starting treatment with most b/tsDMARDs.
- In an attempt to estimate the extent of latent tuberculosis screening, researchers combined claims and electronic health record datasets to evaluate 2853 new b/tsDMARD users (mean age, 73 years; 72% women; and 73% non-Hispanic White).
- The primary analysis focused on assessing the proportion of patients screened for latent tuberculosis in the year before starting a new b/tsDMARD.
- A sensitivity analysis evaluated the extent of screening within the 3 years preceding the initiation of a new b/tsDMARD.
- A total of 65.6% of patients received screening for latent tuberculosis in the year before initiating a new b/tsDMARD.
- Screening rates improved only slightly on expanding the window to 3 years, with 72.9% of patients receiving any tuberculosis screening.
- When stratified by drug type, over half of new users of Janus kinase inhibitors and nearly 90% of new users of interleukin-17 inhibitors had not received screening.
- Hispanic patients had lower odds of tuberculosis screening within 1 year than White patients (odds ratio [OR], 0.64; 95% CI, 0.46-0.90), as did those in the highest socioeconomic quartile, compared with the lowest (OR, 0.61; 95% CI, 0.40-0.94).
IN PRACTICE:
“Educational initiatives, team-based care delivery, task shifting, and technological interventions to address observed gaps in patient safety procedures are needed,” the authors wrote.
SOURCE:
The study was led by Eric T. Roberts, PhD, University of California, San Francisco, and published online in Arthritis Care & Research
LIMITATIONS:
The study lacked access to scanned documents or clinical notes, which may have resulted in the omission of a small number of tests that had no Medicare billing. Moreover, the study was restricted to a 3-year lookback period, potentially missing some remote screenings. The findings may have limited generalizability to younger patients or those not dually eligible for Medicare and Medicaid.
DISCLOSURES:
This study was funded by grants from the Agency for Healthcare Research and Quality and the National Institute for Arthritis and Musculoskeletal and Skin Diseases. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
The rates of screening for latent tuberculosis remain suboptimal among new users of biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs), with notable variations by medication type and demographic characteristics.
METHODOLOGY:
- Professional society guidelines recommend screening for tuberculosis before starting treatment with most b/tsDMARDs.
- In an attempt to estimate the extent of latent tuberculosis screening, researchers combined claims and electronic health record datasets to evaluate 2853 new b/tsDMARD users (mean age, 73 years; 72% women; and 73% non-Hispanic White).
- The primary analysis focused on assessing the proportion of patients screened for latent tuberculosis in the year before starting a new b/tsDMARD.
- A sensitivity analysis evaluated the extent of screening within the 3 years preceding the initiation of a new b/tsDMARD.
- A total of 65.6% of patients received screening for latent tuberculosis in the year before initiating a new b/tsDMARD.
- Screening rates improved only slightly on expanding the window to 3 years, with 72.9% of patients receiving any tuberculosis screening.
- When stratified by drug type, over half of new users of Janus kinase inhibitors and nearly 90% of new users of interleukin-17 inhibitors had not received screening.
- Hispanic patients had lower odds of tuberculosis screening within 1 year than White patients (odds ratio [OR], 0.64; 95% CI, 0.46-0.90), as did those in the highest socioeconomic quartile, compared with the lowest (OR, 0.61; 95% CI, 0.40-0.94).
IN PRACTICE:
“Educational initiatives, team-based care delivery, task shifting, and technological interventions to address observed gaps in patient safety procedures are needed,” the authors wrote.
SOURCE:
The study was led by Eric T. Roberts, PhD, University of California, San Francisco, and published online in Arthritis Care & Research
LIMITATIONS:
The study lacked access to scanned documents or clinical notes, which may have resulted in the omission of a small number of tests that had no Medicare billing. Moreover, the study was restricted to a 3-year lookback period, potentially missing some remote screenings. The findings may have limited generalizability to younger patients or those not dually eligible for Medicare and Medicaid.
DISCLOSURES:
This study was funded by grants from the Agency for Healthcare Research and Quality and the National Institute for Arthritis and Musculoskeletal and Skin Diseases. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
Do Organophosphate Esters Increase Thyroid Disease Risk?
TOPLINE:
, bis(2-chloroethyl) phosphate (BCEP) being the main contributor.
METHODOLOGY:
- Prior studies have reported that OPEs — used in building materials, electronic products, furniture, and textiles — may interfere with thyroid function, hinting at a possible association of OPEs with thyroid disease.
- Researchers assessed the association between OPE exposure and the risk for thyroid disease using data from the 2011-2014 US National Health and Nutrition Examination Survey cycle.
- They included 2449 participants (mean age, 46 years; half of whom were women) who had complete values for seven OPE metabolites through urinalysis and completed questionnaires regarding the presence of thyroid disease.
- The seven OPE metabolites assessed in this study were diphenyl phosphate (DPHP), bis(1,3-dichloro-2-propyl) phosphate, bis(1-chloro-2-propyl) phosphate, BCEP, dibutyl phosphate, dibenzyl phosphate, and 2,3,4,5-tetrabromobenzoic acid.
- Several mixed exposure models were used to investigate the associations between the risk for thyroid disease and exposure to individual and mixed OPEs.
TAKEAWAY:
- A history of thyroid disease was self-reported by 228 participants.
- In one model, the risk for thyroid disease was 57% higher in people in the highest vs the lowest tertile of BCEP exposure (P = .005).
- A newer method confirmed the positive association between exposure to mixed OPE metabolites and a higher risk for thyroid disease (odds ratio, 1.03; P = .013), with BCEP (65%) being the main contributing factor, followed by DPHP (35%).
- A model from another new method showed a J-shaped relationship between the risk for thyroid disease and increasing levels of BCEP exposure, in which the risk first dropped but then rose with increasing exposure.
IN PRACTICE:
“The three models in our study provided similar results, with exposure to mixed OPEs having a tendency to increase the risk of thyroid disease and pointing to BCEP as the most significant compound responsible for this trend,” wrote the authors.
SOURCE:
This study was led by Yuxin Lin, from the Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, China, and published online in Frontiers in Endocrinology.
LIMITATIONS:
The cross-sectional design cannot establish a causal relationship between OPE exposure and thyroid disease. The study used unweighted data, which could have limited the generalizability of the findings. Moreover, urine sample measurements were performed only once.
DISCLOSURES:
The study was supported by the Fujian Natural Science Foundation Program and the Scientific Research Program of High-level Talents of Fujian Medical University. The authors declared no potential conflicts of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
, bis(2-chloroethyl) phosphate (BCEP) being the main contributor.
METHODOLOGY:
- Prior studies have reported that OPEs — used in building materials, electronic products, furniture, and textiles — may interfere with thyroid function, hinting at a possible association of OPEs with thyroid disease.
- Researchers assessed the association between OPE exposure and the risk for thyroid disease using data from the 2011-2014 US National Health and Nutrition Examination Survey cycle.
- They included 2449 participants (mean age, 46 years; half of whom were women) who had complete values for seven OPE metabolites through urinalysis and completed questionnaires regarding the presence of thyroid disease.
- The seven OPE metabolites assessed in this study were diphenyl phosphate (DPHP), bis(1,3-dichloro-2-propyl) phosphate, bis(1-chloro-2-propyl) phosphate, BCEP, dibutyl phosphate, dibenzyl phosphate, and 2,3,4,5-tetrabromobenzoic acid.
- Several mixed exposure models were used to investigate the associations between the risk for thyroid disease and exposure to individual and mixed OPEs.
TAKEAWAY:
- A history of thyroid disease was self-reported by 228 participants.
- In one model, the risk for thyroid disease was 57% higher in people in the highest vs the lowest tertile of BCEP exposure (P = .005).
- A newer method confirmed the positive association between exposure to mixed OPE metabolites and a higher risk for thyroid disease (odds ratio, 1.03; P = .013), with BCEP (65%) being the main contributing factor, followed by DPHP (35%).
- A model from another new method showed a J-shaped relationship between the risk for thyroid disease and increasing levels of BCEP exposure, in which the risk first dropped but then rose with increasing exposure.
IN PRACTICE:
“The three models in our study provided similar results, with exposure to mixed OPEs having a tendency to increase the risk of thyroid disease and pointing to BCEP as the most significant compound responsible for this trend,” wrote the authors.
SOURCE:
This study was led by Yuxin Lin, from the Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, China, and published online in Frontiers in Endocrinology.
LIMITATIONS:
The cross-sectional design cannot establish a causal relationship between OPE exposure and thyroid disease. The study used unweighted data, which could have limited the generalizability of the findings. Moreover, urine sample measurements were performed only once.
DISCLOSURES:
The study was supported by the Fujian Natural Science Foundation Program and the Scientific Research Program of High-level Talents of Fujian Medical University. The authors declared no potential conflicts of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
, bis(2-chloroethyl) phosphate (BCEP) being the main contributor.
METHODOLOGY:
- Prior studies have reported that OPEs — used in building materials, electronic products, furniture, and textiles — may interfere with thyroid function, hinting at a possible association of OPEs with thyroid disease.
- Researchers assessed the association between OPE exposure and the risk for thyroid disease using data from the 2011-2014 US National Health and Nutrition Examination Survey cycle.
- They included 2449 participants (mean age, 46 years; half of whom were women) who had complete values for seven OPE metabolites through urinalysis and completed questionnaires regarding the presence of thyroid disease.
- The seven OPE metabolites assessed in this study were diphenyl phosphate (DPHP), bis(1,3-dichloro-2-propyl) phosphate, bis(1-chloro-2-propyl) phosphate, BCEP, dibutyl phosphate, dibenzyl phosphate, and 2,3,4,5-tetrabromobenzoic acid.
- Several mixed exposure models were used to investigate the associations between the risk for thyroid disease and exposure to individual and mixed OPEs.
TAKEAWAY:
- A history of thyroid disease was self-reported by 228 participants.
- In one model, the risk for thyroid disease was 57% higher in people in the highest vs the lowest tertile of BCEP exposure (P = .005).
- A newer method confirmed the positive association between exposure to mixed OPE metabolites and a higher risk for thyroid disease (odds ratio, 1.03; P = .013), with BCEP (65%) being the main contributing factor, followed by DPHP (35%).
- A model from another new method showed a J-shaped relationship between the risk for thyroid disease and increasing levels of BCEP exposure, in which the risk first dropped but then rose with increasing exposure.
IN PRACTICE:
“The three models in our study provided similar results, with exposure to mixed OPEs having a tendency to increase the risk of thyroid disease and pointing to BCEP as the most significant compound responsible for this trend,” wrote the authors.
SOURCE:
This study was led by Yuxin Lin, from the Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, China, and published online in Frontiers in Endocrinology.
LIMITATIONS:
The cross-sectional design cannot establish a causal relationship between OPE exposure and thyroid disease. The study used unweighted data, which could have limited the generalizability of the findings. Moreover, urine sample measurements were performed only once.
DISCLOSURES:
The study was supported by the Fujian Natural Science Foundation Program and the Scientific Research Program of High-level Talents of Fujian Medical University. The authors declared no potential conflicts of interest.
A version of this article first appeared on Medscape.com.