title: Circadian feeding drive of metabolic activity in adipose tissue and not hyperphagia triggers overweight in mice: is there a role of the pentose-phosphate pathway?
abstract: High-fat (HF) diets trigger an increase in adipose tissue and body weight (BW) and disordered eating behavior. Our study deals with the hypothesis that circadian distribution of energy intake is more relevant for BW dynamics than diet composition. Four-week-old mice were exposed for 8 wk to a HF diet and compared with animals receiving control chow. HF mice progressively increased BW, decreased the amount of nocturnal (1800-0900 h) calories (energy or food intake) (30%) and increased diurnal (0900-1800 h) caloric intake (energy or food intake), although total daily intake was identical between groups. Animals were killed at 3-h intervals and plasma insulin, leptin, corticosterone, glucose, and fatty acid levels quantified. Adipose tissue was weighed, and enzymatic activities integral to the pentose phosphate pathway (PPP) assayed in lumbar adipose tissue. Phosphorylated AMP-dependent protein kinase and fatty acid synthase were quantified by Western blotting. In HF mice, there was a shift in the circadian oscillations of plasma parameters together with an inhibition of PPP activity and a decrease in phosphorylated AMP-dependent protein kinase and fatty acid synthase. In a second experiment, HF mice were forced to adhere to a circadian pattern of food intake similar to that in control animals. In this case, BW, adipose tissue, morning plasma parameters and PPP activity appeared to be normal. These data indicate that disordered feeding behavior can trigger BW gain independently of food composition and daily energy intake. Because PPP is the main source of reduced nicotinamide adenine dinucleotide phosphate, we suggest that PPP inhibition might be an early marker of adipose dysfunction in diet-induced obesity.
authors.affiliation: Instituto Pluridisciplinar and Departamento de Farmacología, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
authors.forename: Paula
authors.initials: P
authors.lastname: Stucchi
authors.forename: Marta
authors.initials: M
authors.lastname: Gil-Ortega
authors.forename: Beatriz
authors.initials: B
authors.lastname: Merino
authors.forename: Rocío
authors.initials: R
authors.lastname: Guzmán-Ruiz
authors.forename: Victoria
authors.initials: V
authors.lastname: Cano
authors.forename: Ismael
authors.initials: I
authors.lastname: Valladolid-Acebes
authors.forename: Beatriz
authors.initials: B
authors.lastname: Somoza
authors.forename: Sophie
authors.initials: S
authors.lastname: Le Gonidec
authors.forename: Jesús
authors.initials: J
authors.lastname: Argente
authors.forename: Philippe
authors.initials: P
authors.lastname: Valet
authors.forename: Julie Ann
authors.initials: JA
authors.lastname: Chowen
authors.forename: Marisol
authors.initials: M
authors.lastname: Fernández-Alfonso
authors.forename: Mariano
authors.initials: M
authors.lastname: Ruiz-Gayo
mesh_terms: D000273:Adipose Tissue / Q000502:physiology*; D050154:Adiposity; D000818:Animals; D002940:Circadian Rhythm / Q000502:physiology*; D003345:Corticosterone / Q000097:blood / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage; D004734:Energy Metabolism / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D006963:Hyperphagia / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009249:NADP / Q000378:metabolism; D050177:Overweight / Q000209:etiology*; D010427:Pentose Phosphate Pathway / Q000502:physiology*; D015430:Weight Gain / Q000502:physiology
chemical_list: D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D009249:NADP; D003345:Corticosterone