Isocaloric Fructose Restriction Reduces Serum d-Lactate Concentration in Children With Obesity and Metabolic Syndrome.
J Clin Endocrinol Metab
; 104(7): 3003-3011, 2019 07 01.
Article
en En
| MEDLINE
| ID: mdl-30869790
ABSTRACT
OBJECTIVE:
To investigate the link between dietary sugar consumption and two separate pathogenetic mechanisms associated with metabolic syndrome de novo lipogenesis (DNL) and nonenzymatic glycation. DESIGN ANDPARTICIPANTS:
We assessed changes in serum d-lactate (the detoxification end-product of methylglyoxal) concentration in response to 9 days of isocaloric fructose restriction in 20 children with obesity and metabolic syndrome, and examined correlations with changes in DNL, liver fat, insulin sensitivity, and other metrics of hepatic metabolism.INTERVENTIONS:
Nine days of dietary sugar restriction, with substitution of equal amounts of refined starch. MAIN OUTCOMEMEASURES:
On days 0 and 10, children had laboratory evaluation of d-lactate levels and other analytes, and underwent oral glucose tolerance testing, magnetic resonance spectroscopy to quantify fat depots, and 13C-acetate incorporation into triglyceride (TG) to measure DNL.RESULTS:
d-Lactate was associated with baseline liver fat fraction (P < 0.001) and visceral adipose tissue (P < 0.001) but not with subcutaneous adipose tissue. At baseline, d-lactate was positively correlated with DNL-area under the curve (AUC) (P = 0.003), liver fat fraction (P = 0.02), TG (P = 0.004), and TG/high-density lipoprotein ratio (P = 0.002). After 9 days of isocaloric fructose restriction, serum d-lactate levels reduced by 50% (P < 0.0001), and changes in d-lactate correlated with both changes in DNL-AUC and measures of insulin sensitivity.CONCLUSION:
Baseline correlation of d-lactate with DNL and measures of insulin sensitivity and reduction in d-lactate after 9 days of isocaloric fructose restriction suggest that DNL and nonenzymatic glycation are functionally linked via intermediary glycolysis in the pathogenesis of metabolic syndrome and point to fructose as a key dietary substrate that drives both pathways.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Resistencia a la Insulina
/
Ácido Láctico
/
Síndrome Metabólico
/
Lipogénesis
/
Obesidad Infantil
/
Azúcares de la Dieta
/
Fructosa
/
Hígado
Tipo de estudio:
Prognostic_studies
Límite:
Adolescent
/
Child
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
J Clin Endocrinol Metab
Año:
2019
Tipo del documento:
Article