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congenital hyperinsulinism/obesitas
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Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value.
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Several groups have reported a risk of fetal macrosomia in pregnancies with maternal glucose intolerance which is intermediate between gestational diabetes (GDM) and normal glucose tolerance. The present study was designed to determine whether these pregnancies are also at risk for fetal obesity,
Long-term follow-up of patients with congenital hyperinsulinism in Austria.
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OBJECTIVE
To assess the neurological and clinical long-term outcome of patients diagnosed with congenital hyperinsulinism (CHI) in Austria.
METHODS
Fourteen patients diagnosed with CHI (1978-2000) were investigated retrospectively by reviewing hospital records. Thirteen of them were evaluated with
Congenital hyperinsulinism due to mutations in HNF1A.
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Congenital hyperinsulinism is a rare but significant cause of severe and persistent hypoglycaemia in infancy. Although a biphasic phenotype of congenital hyperinsulinism in infancy followed by Maturity-Onset Diabetes of the Young (MODY) in later life has been established for HNF4A, the existence of
Overweight and increased diabetes susceptibility in neonatally insulin-treated adult rats.
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OBJECTIVE
Since the offspring of gestational diabetic mothers (GD) is at increased risk to develop obesity and diabetogenic disturbances later in life, while pathophysiological mechanisms responsible are unclear, to investigate long-term consequences of neonatal hyperinsulinism occurring
Long-term lanreotide treatment in six patients with congenital hyperinsulinism.
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BACKGROUND
Medical treatment is a substantial therapeutic measure to achieve glycemic control and prevent hypoglycemic brain damage without surgery in patients with congenital hyperinsulinism (CHI). However, only few drugs are available and even fewer are approved as a medical therapy to maintain
Glucose metabolism and neurological outcome in congenital hyperinsulinism.
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Advances in imaging and surgical techniques allow a complete cure for children with focal-type congenital hyperinsulinism (CHI). In contrast, management of diffuse-type CHI remains a matter of controversy. To prevent hypoglycemic brain damage, extensive surgery has been recommended in the past,
Perinatal hyperinsulinism as possible predisposing factor for diabetes mellitus, obesity and enhanced cardiovascular risk in later life.
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The importance of the intrauterine and neonatal metabolic environment as possible teratogenic determinants of predispositions to diabetes, obesity and cardiovascular diseases is discussed. Epidemiological, clinical and experimental results suggest that gestational diabetes or even slightly impaired
Maternal diabetes and perinatal programming.
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Alterations of the intrauterine and neonatal environment may predispose for disorders and diseases throughout later life (perinatal programming). Especially, hormones and nutrients are dose-dependent organizers of the developing organism. Studies in offspring of diabetic mothers (ODM) have
Adult diffuse nesidioblastosis: genetically or environmentally induced?
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Persistent hyperinsulinemic hypoglycemia in adults is usually caused by solitary benign insulinomas. Nesidioblastosis, a term that has been used to designate a functional disorder of the beta cells, is a rare cause of persistent hyperinsulinemic hypoglycemia in adults, but seems to have increased in
A matter of insulin: developmental programming of body weight regulation.
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Alterations of the intrauterine and early postnatal nutritional, metabolic and hormonal environment may cause a predisposition for disorders and diseases throughout later life. Studies in offspring of diabetic mothers (ODM) have decisively contributed to this perception and our understanding of
The diabetic pregnancy, macrosomia, and perinatal nutritional programming.
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Health and diseases are generally perceived to be caused genetically. It is meanwhile accepted, however, that alterations in the intrauterine and early postnatal nutritional, metabolic, and hormonal environment may also predispose to disorders and diseases throughout later life. Studies in the
Clinical PET imaging of insulinoma and beta-cell hyperplasia.
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Persistent hyperinsulinemic hypoglycemia (PHH) is caused by solitary benign insulinoma or hyperplasia of pancreatic beta cells. In infants, PHH is caused by functionally defective hyperplastic beta cells, which are either diffusely or focally distributed in the pancreas. In adults, insulinoma is the
Network analysis: a new approach to study endocrine disorders.
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Systems biology is the study of the interactions that occur between the components of individual cells - including genes, proteins, transcription factors, small molecules, and metabolites, and their relationships to complex physiological and pathological processes. The application of systems biology
Inhibition of insulin secretion as a new drug target in the treatment of metabolic disorders.
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The pattern of insulin release is crucial for regulation of glucose and lipid haemostasis. Deficient insulin release causes hyperglycemia and diabetes, whereas excessive insulin release can give rise to serious metabolic disorders, such as nesidioblastosis (Persistent Hyperinsulinemic Hypoglycemia
Glucokinase mutation-a rare cause of recurrent hypoglycemia in adults: a case report and literature review.
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BACKGROUND
Hypoglycemia occurs frequently in patients both in the inpatient and outpatient settings. While most hypoglycemia unrelated to diabetes treatment results from excessive endogenous insulin action, rare cases involve functional and congenital mutations in glycolytic enzymes of insulin
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