humulin-s and Weight-Gain

The aim of this review is to summarize the clinical efficacy, tolerability and safety data of insulin detemir, and compare its use with that of neutral protamine Hagedorn (NPH) insulin in randomized controlled trials in people with type 1 or type 2 diabetes. A literature search was conducted with PubMed using predefined search terms. Studies were included if they met the following criteria: randomized, controlled trial, comparison of insulin detemir with NPH insulin, non-hospitalized adults aged ≥18 years with either type 1 or type 2 diabetes, and study duration of ≥12 weeks. The following types of studies were excluded: non-randomized controlled trials, studies of mixed cohorts of patients with type 1 or type 2 diabetes that did not report results separately, pharmacokinetic/pharmacodynamic studies, reviews, pooled or meta-analyses or health-economic analyses. Fourteen publications met the inclusion criteria. Nine studies in people with type 1 diabetes and three studies in people with type 2 diabetes, using insulin detemir in a basal-bolus regimen were included. Two studies were in people with type 2 diabetes using insulin detemir with oral antidiabetes medicines. In 14 studies of people with type 1 or type 2 diabetes, insulin detemir treatment provided similar or better glycaemic control, lower within-subject variability, similar or lower frequency of hypoglycaemia and less weight gain when compared with NPH insulin.

Topics: Adult; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Humans; Hyperglycemia; Hypoglycemia; Hypoglycemic Agents; Insulin Detemir; Insulin, Isophane; Insulin, Long-Acting; Insulin, Regular, Human; Isophane Insulin, Human; Randomized Controlled Trials as Topic; Weight Gain

To explore determinants of excessive weight gain after initiation of insulin therapy in type 2 diabetes mellitus (T2DM), in particular variables identified in the pre-insulin phase.. We performed a retrospective observational intervention cohort study, by means of a new user design/ inception cohort concerning n = 5086 patients. We studied determinants of excessive weight gain (5 kg or more) in the first year after initiation of insulin therapy, using both visualization and logistic regression analysis with subsequent receiver operation characteristic (ROC) analyses. Potential determinants pre-, at- and post-insulin initiation were included.. One out of 10 patients (10.0%) gained 5 kg weight or more. The earliest determinants of excessive weight gain were weight change (inversely) and HbA1c change in the two years prior to insulin therapy (p < 0.001). Patients that lost weight parallel with HbA1c rise in the two-years pre-insulin, showed the most pronounced weight gain. Of these patients, roughly one out of five (20.3%) gained 5 kg weight or more.. Clinicians and patients should be alert for excessive weight gain after initiation of insulin, in the case of weight loss prior to insulin therapy initiation, particularly with increasing and prolonged high HbA1c at (and after) insulin initiation.

Topics: Cohort Studies; Diabetes Mellitus, Type 2; Glycated Hemoglobin; Humans; Hypoglycemic Agents; Insulin; Insulin, Regular, Human; Retrospective Studies; Weight Gain

The aim of this study was to compare glycemic control and body mass index standard deviation score (BMI-SDS) before and after implementation of intensive insulin therapy using multiple daily injection (MDI) or continuous subcutaneous insulin infusion (CSII) in adolescents with type 1 diabetes (T1D) attending a large multidisciplinary paediatric diabetes clinic in Australia.. Prospective data were collected for cross-sectional comparison of youth aged 10.0-17.9 years (n = 669) from routine follow-up visits to the diabetes clinic in 2004, 2010, and 2016. Outcome measures included HbA1c; BMI-SDS; and insulin regimen.. BMI-SDS did not increase with the change to intensive insulin therapy despite a doubling in the number of adolescents achieving the recommended glycemic target of <7.0% (53 mmol/mol). HbA1c was not associated with weight gain.

Topics: Adolescent; Blood Glucose; Child; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Glycated Hemoglobin; Humans; Hypoglycemic Agents; Injections, Subcutaneous; Insulin; Insulin, Regular, Human; Prospective Studies; Weight Gain

Fetal macrosomia is associated with perinatal injuries. The purpose of this study was to assess the relationship between fetal insulin, insulin-like Growth factor-1(IGF-1), and macrosomia in a resource-limited setting.. This was a case-control study at tertiary and secondary health facilities in Lagos, Nigeria. One hundred and fifty mother-neonate pairs were recruited, and their socio-demographic and obstetric history was recorded. Fetal cord venous blood was collected at birth, and neonatal anthropometry was measured within 24hrs of life. Insulin and IGF-1 assay were measured with Enzyme-Linked Immunosorbent Assay (ELISA). Pearson's Chi-square was used to assess the association between categorical variables and macrosomia. Spearman's rank correlation of insulin, IGF-1, and fetal anthropometry was performed. Multivariable logistic regression was used to evaluate the association of insulin and IGF-1 with fetal birth weight. A statistically significant level was set at P-value < 0.05.. Macrosomic neonates had mean fetal weight, fetal length, and occipitofrontal circumference (OFC) of 4.15±0.26kg, 50.85±2.09cm and 36.35± 1.22cm respectively. The median Insulin (P = 0.023) and IGF-1 (P < 0.0001) were significantly higher among macrosomic neonates as compared to normal weight babies. Maternal BMI at birth (p = 0.003), neonate's gender (p < 0.001), fetal cord serum IGF-1 (p < 0.001) and insulin assay (P-value = 0.027) were significant predictors of fetal macrosomia. There was positive correlation between cord blood IGF-1 and birth weight (r = 0.47, P-value < 0.001), fetal length (r = 0.30, P-value = 0.0002) and OFC (r = 0.37, P-value < 0.001).. Among participating mother-neonate dyad, maternal BMI at birth, neonate's gender, and fetal cord serum IGF-1 and serum insulin are significantly associated with fetal macrosomia.

Topics: Birth Weight; Case-Control Studies; Female; Fetal Blood; Fetal Macrosomia; Humans; Infant, Newborn; Insulin; Insulin-Like Growth Factor I; Insulin-Like Growth Factor II; Insulin, Regular, Human; Nigeria; Pregnancy; Weight Gain

We previously reported an increased risk of being small for gestational age (SGA) and a decreased risk of being large for gestational age (LGA) after in utero exposure to metformin compared with insulin exposure. This follow-up study investigated if these observations remain when metformin exposure (henceforth, metformin cohort) is compared with non-pharmacological antidiabetic treatment of gestational diabetes mellitus (GDM; naïve cohort), instead of insulin. RESEARCH DESIGN AND METHODS : This was a Finnish population register-based cohort study from singleton children born during 2004-2016. Birth outcomes from metformin cohort (n=3964) and the naïve cohort (n=82 675) were used in the main analyses. Additional analyses were conducted in a subcohort, restricting the metformin cohort to children of mothers with GDM only (n=2361). Results were reported as inverse probability of treatment weighted OR (wOR), with the naïve cohort as reference. RESULTS  : No difference was found for the outcome of SGA between the cohorts in the main analyses (wOR 0.97, 95% CI 0.73 to 1.27) or in the additional analyses (wOR 1.01, 95% CI 0.75 to 1.37). No difference between the cohorts was found for the risk of LGA (wOR 0.91, 95% CI 0.75 to 1.11) in the main analyses but a decreased risk was observed in the additional analyses (wOR 0.72, 95% CI 0.56 to 0.92). CONCLUSIONS : This follow-up study found no increase in the risk of SGA or LGA after in utero exposure to metformin, compared with drug-naïve GDM. The decreased risk of LGA in mothers with GDM may suggest residual confounding. The lack of increased SGA risk aligns with findings from studies using metformin in non-diabetic pregnancies. In contrast, lower birth weight and increased SGA birth risk were observed in GDM pregnancies for metformin versus insulin. Metformin should be avoided with emerging growth restriction in utero. The interplay of intrauterine hyperglycemia and pharmacological treatments needs further assessment.

Topics: Child; Cohort Studies; Diabetes, Gestational; Female; Follow-Up Studies; Humans; Infant, Newborn; Insulin; Insulin, Regular, Human; Metformin; Pregnancy; Weight Gain