FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W127980303> ?p ?o ?g. }

• W127980303 endingPage "183" @default.
• W127980303 startingPage "161" @default.
• W127980303 abstract "To examine the glucoregulatory responses to stress and their impact on diabetes, we used the following models of stress: A) Hypoglycemia; B) Epinephrine infusion; C) intracerebroventricular (ICV) injection of carbachol, an analog of acetylcholine. A) Hypoglycemia induces release of all counterregulatory hormones. During acute hypoglycemia, glucose production increases initially mainly due to glucagon release but eventually also due to a very large increment in catecholamines. In newborn dogs, neither epinephrine nor glucagon respond to a decrease in plasma glucose. This lack of a safeguard against hypoglycemia may indicate that the brain in pups is less dependent on a normal supply of glucose as a fuel, than in adult dogs. Counterregulation is enhanced when the effects of endogenous opiates are blocked by naloxone, indicating that endogenous opiates play a regulatory role during hypoglycemia. However, beta-endorphins which can be released with epinephrine during various stress situations, potentiate the peripheral effect of epinephrine. Glucoregulatory responses, even to slight changes in plasma glucose, are greatly enhanced during glucocorticoid treatment. This apparently reflects the greater sensitivity of the liver to glucagon. In diabetic dogs, similar to human diabetics, the glucagon response is abolished and the response of the catecholamines is partially decreased. On the basis of histological studies, we proposed that the deficient glucagon response in diabetes could be related to an increase in the somatostatin-glucagon ratio in the diabetic pancreas. This ratio is further augmented when normoglycemia is maintained with insulin. In response to a decrease in plasma glucose, there is a biphasic increment in glucose production in normal dogs, which is missing in diabetes. When normoglycemia is restored in diabetic dogs with phlorizin treatment, the second but not the first increment in glucose production is restored. We postulated, therefore, that the toxic effect of hyperglycemia, in addition to the lack of glucagon response, is the main reason why in diabetes, glucose production cannot respond promptly to a decrease in plasma glucose. The low rate of metabolic clearance of glucose seen in diabetes in the post-absorptive state, also reflects, at least in part, the toxic effect of glucose, because with acute normalization of glucose with phlorizin, metabolic glucose clearance substantially improves. Hyperglycemia is the main reason for the decreased number of glucose transporters in diabetic muscle. B) Epinephrine infusion in normal dogs mimics some effects of stress, in that it increases glucose production, inhibits metabolic glucose clearance and increases lipolysis. These metabolic effects of epinephrine are independent of glucagon release.(ABSTRACT TRUNCATED AT 400 WORDS)" @default.
• W127980303 created "2016-06-24" @default.
• W127980303 creator A5014612757 @default.
• W127980303 creator A5017144971 @default.
• W127980303 creator A5035148372 @default.
• W127980303 creator A5054593546 @default.
• W127980303 creator A5065151883 @default.
• W127980303 creator A5087798071 @default.
• W127980303 creator A5088832261 @default.
• W127980303 date "1991-01-01" @default.
• W127980303 modified "2023-09-27" @default.
• W127980303 title "Effect of Stress on Glucoregulation in Physiology and Diabetes" @default.
• W127980303 cites W1600232156 @default.
• W127980303 cites W1835275538 @default.
• W127980303 cites W1951067575 @default.
• W127980303 cites W1966946242 @default.
• W127980303 cites W1976487561 @default.
• W127980303 cites W1980093709 @default.
• W127980303 cites W1983777004 @default.
• W127980303 cites W1985645871 @default.
• W127980303 cites W1988160703 @default.
• W127980303 cites W1991639257 @default.
• W127980303 cites W2000274497 @default.
• W127980303 cites W2004009337 @default.
• W127980303 cites W2006779085 @default.
• W127980303 cites W2011155901 @default.
• W127980303 cites W2012650844 @default.
• W127980303 cites W2021982751 @default.
• W127980303 cites W2024472149 @default.
• W127980303 cites W2025157980 @default.
• W127980303 cites W2025374971 @default.
• W127980303 cites W2030958701 @default.
• W127980303 cites W2031323777 @default.
• W127980303 cites W2033052007 @default.
• W127980303 cites W2046700227 @default.
• W127980303 cites W2051877725 @default.
• W127980303 cites W2052586828 @default.
• W127980303 cites W2059802140 @default.
• W127980303 cites W2062646820 @default.
• W127980303 cites W2063841538 @default.
• W127980303 cites W2077677098 @default.
• W127980303 cites W2079516975 @default.
• W127980303 cites W2082022468 @default.
• W127980303 cites W2087529101 @default.
• W127980303 cites W2091241147 @default.
• W127980303 cites W2096329362 @default.
• W127980303 cites W2104320924 @default.
• W127980303 cites W2107037674 @default.
• W127980303 cites W2123756927 @default.
• W127980303 cites W2146533011 @default.
• W127980303 cites W2152002836 @default.
• W127980303 cites W2152602918 @default.
• W127980303 cites W2171055934 @default.
• W127980303 cites W2254848093 @default.
• W127980303 cites W2257717193 @default.
• W127980303 cites W2339688055 @default.
• W127980303 cites W2339779641 @default.
• W127980303 cites W2414180463 @default.
• W127980303 cites W2414233537 @default.
• W127980303 cites W2431468329 @default.
• W127980303 cites W2437396817 @default.
• W127980303 cites W4237667375 @default.
• W127980303 cites W4239374267 @default.
• W127980303 cites W4240307599 @default.
• W127980303 cites W4241072508 @default.
• W127980303 cites W4241882260 @default.
• W127980303 cites W4245233052 @default.
• W127980303 cites W4248152591 @default.
• W127980303 cites W4248953975 @default.
• W127980303 cites W2005545607 @default.
• W127980303 doi "https://doi.org/10.1007/978-1-4684-5931-9_13" @default.
• W127980303 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/1927681" @default.
• W127980303 hasPublicationYear "1991" @default.
• W127980303 type Work @default.
• W127980303 sameAs 127980303 @default.
• W127980303 citedByCount "14" @default.
• W127980303 countsByYear W1279803032012 @default.
• W127980303 countsByYear W1279803032014 @default.
• W127980303 countsByYear W1279803032015 @default.
• W127980303 countsByYear W1279803032016 @default.
• W127980303 crossrefType "book-chapter" @default.
• W127980303 hasAuthorship W127980303A5014612757 @default.
• W127980303 hasAuthorship W127980303A5017144971 @default.
• W127980303 hasAuthorship W127980303A5035148372 @default.
• W127980303 hasAuthorship W127980303A5054593546 @default.
• W127980303 hasAuthorship W127980303A5065151883 @default.
• W127980303 hasAuthorship W127980303A5087798071 @default.
• W127980303 hasAuthorship W127980303A5088832261 @default.
• W127980303 hasConcept C126322002 @default.
• W127980303 hasConcept C134018914 @default.
• W127980303 hasConcept C16613235 @default.
• W127980303 hasConcept C170493617 @default.
• W127980303 hasConcept C2775859304 @default.
• W127980303 hasConcept C2778563252 @default.
• W127980303 hasConcept C2778750930 @default.
• W127980303 hasConcept C2779306644 @default.
• W127980303 hasConcept C2780668416 @default.
• W127980303 hasConcept C2781063702 @default.

• next