Tänään julkaistussa tutkimuksessa sokerirasituskoe aiheutti ylipainoisille insuliiniresistenteille lapsille ja nuorille suuremman glukagonivasteen ja pienemmän GLP-1 -vasteen kuin verrokkiryhmälle.
Edellinen merkitsee sitä, että ylipainoisilla insuliiniresistenteillä lapsilla ja nuorilla suuren glykeemisen kuorman ateria eli runsaasti hiillihydraatteja sisältävä ateria nostaa verensokerin korkeammalle ja jälkimmäinen sitä, että tällainen ateria tekee heidät vähemmän kylläiseksi.
Isompaa verensokerin pompsahdusta seuraa isompi pudotus ja pian on taas nälkä. Kun ateria ei tee kylläiseksi, tulee syödyksi enemmän. Lihomiskierre jatkuu ja insuliiniresistenssi pahenee.
Sitä ei varmaan tarvitse edes sanoa, mutta sanon kuitenkin, että ratkaisu olisi tetenkin hiilarirajoitus.
https://pubmed.ncbi.nlm.nih.gov/38087928/Lainaa:
2023 Dec 13 Online ahead of print.
Altered glucagon and GLP-1 responses to oral glucose in children and adolescents with obesity and insulin resistance
DOI: 10.1210/clinem/dgad728
Abstract
Context: Pediatric obesity is characterized by insulin resistance, yet it remains unclear whether insulin resistance contributes to abnormalities in glucagon and incretin secretion.
Objective: To examine whether fasting and stimulated glucagon, GLP-1, and GIP concentrations differ between children and adolescents with obesity and insulin resistance (OIR), obesity and normal insulin sensitivity (OIS), and controls with normal weight (NW).
Methods: 80 (34 boys) children and adolescents, aged 7-17 years with OIR (n=22), OIS (n=22), and NW (n=36) underwent an oral glucose tolerance test with measurements of serum insulin, plasma glucose, glucagon, total GLP-1, and total GIP. Homeostatic model assessment of insulin resistance (HOMA-IR), single point insulin sensitivity estimator (SPISE), Matsuda index, insulinogenic index (IGI), and oral disposition index (ODI) were calculated.
Results: Fasting concentrations of glucagon and GLP-1 were higher in the OIR-group, with no significant differences for GIP. The OIR-group had higher glucagon total area under the curve (tAUC0-120) and lower GLP-1 incremental AUC (iAUC0-120), with no significant differences for GIP iAUC0-120. Higher fasting glucagon was associated with higher HOMA-IR, lower Matsuda index, lower SPISE, higher IGI, and higher plasma alanine transaminase, whereas higher fasting GLP-1 was associated with higher HOMA-IR, lower Matsuda index, and lower ODI. Higher glucagon tAUC0-120 was associated lower SPISE and lower Matsuda index, whereas lower GLP-1 iAUC0-120 was associated with a higher HOMA-IR, lower Matsuda index, and lower ODI.
Conclusions: The OIR-group had elevated fasting concentrations of glucagon and GLP-1, and higher glucagon, but lower GLP-1 responses during an OGTT compared to the OIS- and NW-groups. In contrast, the OIS-group had similar hormone responses to the NW-group.
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