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Objective :In children born small for gestational age (SGA), the relationship betweengrowth hormone (GH) treatment and insulin resistance (IR) has only been investigated fora short period, necessitating a longer observation period. This study aimed to evaluate thelong‐term (10 years) effect of GH to SGA‐children on IR and safety during treatment.Design:This was a multicenter observational study.Patients:SGA‐children who received GH treatment in Spain (stratified by Tanner‐stage and age at GH onset [two groups:≤6 years old or >6 years old]).Measurements:The analysed variables (yearly measures) included auxologic, meta-bolic (insulin‐like growth factor‐1 (IGF‐1), height velocity [HV], weight and homeo-static model assessment‐IR [HOMA‐IR]) and safety data. Data were collectedprospectively (since the study approval: 2007) and retrospectively (since the initia-tion of GH treatment: 2005–2007).Results:A total of 389 SGA children (369 Tanner‐I) were recruited from 27 centres.The mean age (standard deviation) of the children at GH treatment onset was 7.2(2.8) years old. IGF‐1 (standard deviation score [SDS]) and HOMA‐IR values tendedto increase until the sixth year of GH‐treatment, with significant differences beingobserved only during the first year, while these remained stable in the later years(within normal ranges). Height (SDS) increased significantly (basal:−3.0; tenthyear:−1.13), and the maximum HV (SDS) occurred during the first year (2.75 ± 2.39).Conclusions:HOMA‐IR values increased significantly in SGA‐children during thefirst year of GH‐treatment, remained stable and were within normal ranges in allcases. Our 10‐year data suggests that long‐term GH treatment does not promote IRand is well‐tolerated, safe and effective.

Objective :In children born small for gestational age (SGA), the relationship betweengrowth hormone (GH) treatment and insulin resistance (IR) has only been investigated fora short period, necessitating a longer observation period. This study aimed to evaluate thelong‐term (10 years) effect of GH to SGA‐children on IR and safety during treatment.Design:This was a multicenter observational study.Patients:SGA‐children who received GH treatment in Spain (stratified by Tanner‐stage and age at GH onset [two groups:≤6 years old or >6 years old]).Measurements:The analysed variables (yearly measures) included auxologic, meta-bolic (insulin‐like growth factor‐1 (IGF‐1), height velocity [HV], weight and homeo-static model assessment‐IR [HOMA‐IR]) and safety data. Data were collectedprospectively (since the study approval: 2007) and retrospectively (since the initia-tion of GH treatment: 2005–2007).Results:A total of 389 SGA children (369 Tanner‐I) were recruited from 27 centres.The mean age (standard deviation) of the children at GH treatment onset was 7.2(2.8) years old. IGF‐1 (standard deviation score [SDS]) and HOMA‐IR values tendedto increase until the sixth year of GH‐treatment, with significant differences beingobserved only during the first year, while these remained stable in the later years(within normal ranges). Height (SDS) increased significantly (basal:−3.0; tenthyear:−1.13), and the maximum HV (SDS) occurred during the first year (2.75 ± 2.39).Conclusions:HOMA‐IR values increased significantly in SGA‐children during thefirst year of GH‐treatment, remained stable and were within normal ranges in allcases. Our 10‐year data suggests that long‐term GH treatment does not promote IRand is well‐tolerated, safe and effective.

Objective :In children born small for gestational age (SGA), the relationship betweengrowth hormone (GH) treatment and insulin resistance (IR) has only been investigated fora short period, necessitating a longer observation period. This study aimed to evaluate thelong‐term (10 years) effect of GH to SGA‐children on IR and safety during treatment.Design:This was a multicenter observational study.Patients:SGA‐children who received GH treatment in Spain (stratified by Tanner‐stage and age at GH onset [two groups:≤6 years old or >6 years old]).Measurements:The analysed variables (yearly measures) included auxologic, meta-bolic (insulin‐like growth factor‐1 (IGF‐1), height velocity [HV], weight and homeo-static model assessment‐IR [HOMA‐IR]) and safety data. Data were collectedprospectively (since the study approval: 2007) and retrospectively (since the initia-tion of GH treatment: 2005–2007).Results:A total of 389 SGA children (369 Tanner‐I) were recruited from 27 centres.The mean age (standard deviation) of the children at GH treatment onset was 7.2(2.8) years old. IGF‐1 (standard deviation score [SDS]) and HOMA‐IR values tendedto increase until the sixth year of GH‐treatment, with significant differences beingobserved only during the first year, while these remained stable in the later years(within normal ranges). Height (SDS) increased significantly (basal:−3.0; tenthyear:−1.13), and the maximum HV (SDS) occurred during the first year (2.75 ± 2.39).Conclusions:HOMA‐IR values increased significantly in SGA‐children during thefirst year of GH‐treatment, remained stable and were within normal ranges in allcases. Our 10‐year data suggests that long‐term GH treatment does not promote IRand is well‐tolerated, safe and effective.

Background: Liver is a vital organ that plays a major role in glucose production and regulationthroughout the body (Musso et al., 2012). Liver disease has long been linked with insulin resistance (IR), dating back to 1906 (Megyesi et al., 1967). IR has been found to be prevalent in a range of liver diseases, including chronic Hepatitis C Virus (HCV), hemochromatosis, and alcoholic liver disease (Goswami et al., 2014). Liver disease is highly prevalent in the United States population with 30 million people (or one out of ten Americans) suffering from some type of liver disease (Peery et al., 2015). Although research demonstrates a significant relationship between liver disease and IR, the University of Arizona (UA) hepatology clinic does not currently screen liver disease patients for IR. Homeostatic model assessment for insulin resistance (HOMA-IR) score is used to study IR in non-insulin resistant population. HOMA-IR score is calculated using formula fasting plasma glucose (mmol/l) times fasting serum insulin (mU/l) divided by 22.5 (Bonora et al., 2002). Low HOMA-IR (HOMA< 2.0) values indicate high insulin sensitivity, whereas high HOMA-IR (HOMA> 2.0) values indicate low insulin sensitivity (insulin resistance) (Bonora et al., 2002). Objective: The purpose of this quality improvement (QI) project is to show the prevalence of IR in euglycemic liver disease patients at the UA hepatology clinic by using their HOMA-IR scores as a screening tool. By screening euglycemic liver disease patients for IR based on their HOMA-IR score, providers at the UA hepatology clinic can prevent liver disease progression and complications associated with IR early on. By doing so, the providers can improve the quality of care for liver disease patients. An essential part of calculating HOMA-IR is the availability of labs (serum glucose and serum insulin). A part of this QI project is to determine if the UA hepatology clinic has necessary labs to calculate HOMA-IR for euglycemic liver dise

This study investigated the relationship between insulin-resistance and constituent components of executive function in a sample of neurologically intact older adult subjects using the homeostasis model assessment (HOMA-IR) and latent factors of working memory, cognitive control and processing speed derived from confirmatory factor analysis. Low-density lipoprotein (LDL), mean arterial pressure (MAP), along with body mass index (BMI) and white matter hypointensity (WMH) were used to control for vascular risk factors, adiposity and cerebrovascular injury. The study included 119 elderly subjects recruited from the University of California, San Francisco Memory and Aging Center. Subjects underwent neuropsychological assessment, fasting blood draw and brain magnetic resonance imaging (MRI). Partial correlations and linear regression models were used to examine the HOMA-IR-executive function relationship. Pearson correlation adjusting for age showed a significant relationship between HOMA-IR and working memory (rp = -.18; p = .047), a trend with cognitive control (rp = -.17; p = .068), and no relationship with processing speed (rp = .013; p = .892). Linear regression models adjusting for demographic factors (age, education, and gender), LDL, MAP, BMI, and WMH indicated that HOMA-IR was negatively associated with cognitive control (r = -.256; p = .026) and working memory (r = -.234; p = .054). These results suggest a greater level of peripheral insulin-resistance is associated with decreased cognitive control and working memory. After controlling for demographic factors, vascular risk, adiposity and cerebrovascular injury, HOMA-IR remained significantly associated with cognitive control, with working memory showing a trend. These findings substantiate the insulin-resistance-executive function hypothesis and suggest a complex interaction, demonstrated by the differential impact of insulin-resistance on processing speed and specific aspects of executive function.