title: Consumption of sucrose from infancy increases the visceral fat accumulation, concentration of triglycerides, insulin and leptin, and generates abnormalities in the adrenal gland.
abstract: Consumption of sugar-sweetened beverages promotes the development of metabolic syndrome (MetS) and type 2 diabetes mellitus in humans. One factor related to the appearance of MetS components is the dysfunction of the adrenal gland. In fact, the experimental generation of hyperglycemia has been associated with morphological and microvascular changes in the adrenal glands of rats. We hypothesized that high sucrose consumption from infancy promotes histological disruption of the adrenal glands associated with the appearance of metabolic syndrome indicators. Male Wistar rats were separated at weaning (21 days old) into two groups: free access to tap water (control group, C) or 30 % sucrose diluted in water (sugar-fed group). After 12 weeks, high sucrose consumption promoted an increase in visceral fat accumulation, adipose cell number, and insulin resistance. Also, a rise in the concentration of triglycerides, very low-density lipoprotein, insulin and leptin was observed. In control rats, a histomorphometric asymmetry between the right and left adrenal glands was found. In the sugar-fed group, sucrose consumption produced a major change in adrenal gland asymmetry. No changes in corticosterone serum level were observed in either group. Our results suggest that a high sucrose liquid-diet from early life alters the morphology of adrenocortical zones, leading to MetS indicators.
authors.affiliation: Doctorado en Ciencias Biológicas, Universidad Autónoma de Tlaxcala, Tlaxcala, México.
authors.forename: Yadira
authors.initials: Y
authors.lastname: Díaz-Aguila
authors.affiliation: Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México.
authors.forename: Francisco
authors.initials: F
authors.lastname: Castelán
authors.affiliation: Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México.
authors.forename: Estela
authors.initials: E
authors.lastname: Cuevas
authors.affiliation: Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México, México.
authors.forename: Elena
authors.initials: E
authors.lastname: Zambrano
authors.affiliation: Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México.|Departamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, México.
authors.forename: Margarita
authors.initials: M
authors.lastname: Martínez-Gómez
authors.affiliation: Houston Methodist Research Institute, Houston, TX, USA.
authors.forename: Alvaro
authors.initials: A
authors.lastname: Muñoz
authors.affiliation: Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México.
authors.forename: Jorge
authors.initials: J
authors.lastname: Rodríguez-Antolín
authors.affiliation: Centro Tlaxcala de Biología de la Conducta, Universidad Autónoma de Tlaxcala, Tlaxcala, México. lettita2@yahoo.com.
authors.forename: Leticia
authors.initials: L
authors.lastname: Nicolás-Toledo
mesh_terms: D000311:Adrenal Glands / Q000098:blood supply* / Q000473:pathology*; D000367:Age Factors; D000818:Animals; D019422:Dietary Sucrose / Q000009:adverse effects*; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D007328:Insulin / Q000378:metabolism*; D050152:Intra-Abdominal Fat / Q000378:metabolism*; D020738:Leptin / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D055806:Microvessels / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D019422:Dietary Sucrose; D007328:Insulin; D020738:Leptin; D014280:Triglycerides
keywords: Adrenal gland; Insulin; Leptin; Triglycerides; Visceral fat