Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed glucagon stimulation tests in 59 normally growing siblings of children who died from sudden infant death syndrome. These investigations were performed to exclude a possible metabolic disorder (found in 4 siblings) as an underlying cause of sudden infant death syndrome. The remaining 55 siblings (32 boys and 23 girls) provide control data for this age range. Testing was performed at 0800 h after a 15-h fast. The median age was 98 days (range, 13-349 days). Plasma glucose and serum cortisol, insulin, and GH were determined before and 30, 60, 90, 120, 150, and 180 min after im injection of 0.1 mg/kg glucagon. No side-effects were observed during the procedure. Asymptomatic hypoglycemia was noted in 11% of the infants at least once between 120-180 min. Basal and peak GH concentrations were greater than 10 micrograms/L in 31% and 80% of the infants, respectively. There was a significant negative correlation between age and basal GH concentration [Spearman's rank correlation coefficient (rs) = -0.37; P < 0.01]. There was a significant correlation between age and glucagon-stimulated cortisol at 120, 150, and 180 min (rs) = 0.41; P < 0.005), but not between age and changes in glucose levels. There was no significant correlation between age and basal cortisol or peak GH concentrations and no difference between boys and girls for any of the variables studied. In conclusion, the glucagon stimulation test is well tolerated in very young subjects. The peak GH response to glucagon injection is independent of age between 0.5-12 months. The age-related increase in the glucagon-stimulated cortisol response despite a similar decrease in glucose suggests the existence of a postnatal maturation in the response of the pituitary-adrenal axis to stress.
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PMID:Glucose, growth hormone, cortisol, and insulin responses to glucagon injection in normal infants, aged 0.5-12 months. 755 92

The pancreatic islets from 112 infants (66 males and 46 females) who died of SIDS during the years 1990-1992 have been studied. The control group consisted of endocrine pancreas tissue from 19 infants who died of a clear cause of death (pneumonia, drowning, sepsis, etc.). The mean age of the SIDS group was 5.1 months. We found histologically normally developed organs in all the SIDS cases. By evaluating the relative endocrine cell area of the pancreas by immunohistochemical investigations, A-cells were found to make up 10-30%, B-cells 30-60%, D-cells 10-30% and pancreatic polypeptide cells less than 10% in the SIDS group and in the controls with a small increase in glucagon and insulin cells among SIDS cases. The morphometric evaluation revealed that cell enlargement and cytoplasm shrinking occurred slightly more often in the SIDS group than in the control group. The diameter of the islets was normal and the maximal volume was not enlarged. The results did not show significant differences so that a relationship between alterations of the endocrine pancreas and sudden infant death syndrome could not be demonstrated.
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PMID:Morphology, immunohistochemistry and morphometry of pancreatic islets in cases of sudden infant death syndrome (SIDS). 927 44

We studied glucagon-induced growth hormone secretion in 9 patients with apnea of infancy and in 55 siblings of children who had died of sudden infant death syndrome, who were included as a comparison group. We observed a 33% decrease in growth hormone secretion in patients with apnea of infancy. However, linear growth remained normal. This finding could be related to either repeated episodes of hypoxia or to abnormal maturation of the autonomous nervous system.
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PMID:Decreased growth hormone response to glucagon in infants after an apnea of infancy. 954

Sudden infant death syndrome (SIDS) remains a perplexing diagnosis with conflicting laboratory investigation and lack of a biologically plausible aetiology. Investigations into the endogenous vasoactive neuropeptides, including pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are revealing the critical role these substances have in homeostasis including thermo- and cardiovascular regulation. For example, studies in PACAP receptor-deficient mice have revealed sudden neonatal death attributed to respiratory control defects, possibly due to mutations in genes encoding components of PACAP signalling pathways. PACAP and VIP belong to the secretin/glucagon superfamily of hormones and function as vasoactive neuropeptides. They act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to small peptide fragments. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. Vasoactive neuropeptides have a known role in thermoregulation and deficiency states are associated with higher neonatal death rates in rats. PACAP plays a significant role in carbohydrate and lipid metabolism and impairment of functioning has potentially serious consequences. It is postulated PACAP and VIP receptors in brain may become compromised through autoimmune phenomena resulting in cardio-respiratory dysfunction and death. This paper discusses the potential role of certain vasoactive neuropeptides in causing autoimmune responses in susceptible infants predisposing them to SIDS.
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PMID:Is sudden infant death syndrome (SIDS) an autoimmune disorder of endogenous vasoactive neuropeptides? 1508 84

An ongoing study at the University of Nebraska-Lincoln (which included 14 batches of gilts; n = 90 gilts/batch) demonstrated that energy restriction during the developmental period of a gilt increases longevity and may also have beneficial effects on progeny health and growth, particularly, parity 1 progeny. Therefore, we hypothesized that energy restriction during gilt development may affect milk nutrient profile, milk oligosaccharides (OS), and postnatal progeny biomarkers. During the development period, batch 14 gilts (n = 128, 8 gilts/pen) were fed 3 dietary treatments including the following: 1) Control diet formulated to NRC (2012) specifications (CTL); 2) Restricted (20% energy restriction via addition of 40% soy hulls; RESTR); and 3) CTL diet plus addition of crystalline amino acids equivalent to the SID Lys:ME of the RESTR diet (CTL+). All diets were fed ad libitum and applied in a 3-phase feeding regimen during gilt development (days 123 to 230 of age). Average daily feed intake was used to estimate daily metabolizable energy intake (Mcal/d) during each phase (Phase 1: 10.13, 6.97, 9.95; Phase 2: 11.25, 8.05, 10.94; and Phase 3: 9.47, 7.95,11.07) for CTL, RESTR, and CTL+, respectively. After 230 d of age, gilts were bred and fed a common diet. Milk samples were collected from batch 14 gilts (n = 7 per treatment) on days 0 and 14 postfarrowing for compositional analysis of N, CP, dry matter (DM), GE, insulin, and OS. Piglet blood samples (n = 6 piglets/gilt) were obtained on days 1 and 15 postfarrowing for quantification of glucagon-like peptide-2 (GLP-2) and insulin. No effects of developmental diet were observed for milk N, CP, DM, or GE; however, N, CP, DM, and insulin were increased (P < 0.05) on day 1 compared with day 14. A total of 61 different milk OS were identified. Milk OS profile was significantly different for neutral and acidic OS (P < 0.05) on day 0, but there were no significant differences on day 14. For piglet GLP-2, a treatment by day interaction was observed (P < 0.009); specifically, on day 1 GLP concentrations were greater (P < 0.001) in CTL+ compared with RESTR (6.73 vs. 1.21 ng/mL). For serum insulin, a treatment by day interaction was observed (P < 0.01); specifically, insulin in RESTR progeny was greater (P < 0.03) than CTL on day 1. In conclusion, nutritional management of the developing gilt may affect milk nutrient composition, milk OS profile, and piglet serum biomarkers.
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PMID:Effects of energy restriction during gilt development on milk nutrient profile, milk oligosaccharides, and progeny biomarkers. 2986 Mar 39