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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The growth hormone (GH)-insulin-like growth factor (IGF) axis and insulin are major anabolic effectors in promoting weight gain and linear growth. These two anabolic systems are interlinked at many levels, thus abnormalities in one of these systems effect the other causing disordered metabolic homeostasis. Insufficient portal insulinization in insulin dependent diabetes mellitus (IDDM) results in hepatic GH resistance and increased production of IGF-binding proteins-1 (IGFBP-1) and IGFBP-2. GH resistance is reflected by decreased hepatic IGF-I production. In addition, changes in other GH-dependent proteins are also observed in IDDM. Increased proteolysis of IGFBP-3 results in reduction of intact IGFBP-3. Serum ALS levels are also slightly diminished in untreated diabetic patients. Hepatic resistance to GH is, at least in part, caused by diminished GH receptors as reflected by diminished circulating GHBP levels. In addition, there is also evidence from experimental and human studies suggesting post-receptor defect(s) in GH action. As a result of these changes, circulating total and free IGF-I levels are decreased during insulinopenia. Lack of negative feed-back effect of IGF-I on GH secretion causes GH hypersecretion which increases hyperglycemia by decreasing sensitivity to insulin. GH hypersecretion in poorly controlled diabetic patients may play a role in the pathogenesis of diabetic vascular complications. Most of these abnormalities in the GH-IGF axis in diabetes are reversed by effective insulinization of the patient. Addition of IGF-I treatment to insulin in adolescents with IDDM allows correction of GH hypersecretion, improves insulin sensitivity and glycemic control, and decreases insulin requirements. The effect of IGF-I treatment on diabetic complications has yet to be seen.
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PMID:Alterations in the growth hormone-insulin-like growth factor axis in insulin dependent diabetes mellitus. 1022 99

Though children with type 1 diabetes mellitus (T1DM) are often tall at the time of diagnosis, they may experience growth retardation, pubertal delay or both, which may be due to poor glycemic control, associated diseases or chronic complications. Factors affecting growth include: gender, genetic environment, age at diagnosis, diabetes duration, puberty, metabolic control, and status of growth hormone (GH), insulin-like growth factors (IGFs), and IGF binding proteins (IGFBPs). Insulin regulates expression of hepatic GH receptors, affects IGFs and IGFBPs synthesis by modulating GH postreceptor events, and significantly increases IGF-I bioactivity. Low portal insulin seen in T1DM leads to GH hypersecretion, low circulating IGF-I and IGFBP-3, and high circulating IGFBP-1. Newly diagnosed T1DM patients have decreased GHBP which can be restored with insulin therapy. Growth velocity should be appropriate for the age of the child/adolescent, and the mid-parental height. Height, weight and blood pressure (BP) should be measured and plotted on a growth chart at least 2-3 times a year. Puberty should also be assessed annually. Following precautions are to be taken in T1DM children: checking for pubertal onset and ensuring it is not delayed, testing early when growth falters (hypothyroidism/celiac disease/puberty/other conditions), aiming for best possible metabolic control (multidose regimens, regardless of type of insulin), and encouraging dietary calcium and protein, exposure to sunlight, Vitamin D supplements and exercise.
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PMID:Growth disorders in type 1 diabetes: an Indian experience. 2594 56