OBJECTIVE: One major risk factor for childhood overweight is maternal obesity. The underlying molecular mechanisms are ill-defined, and effective prevention strategies are missing. METHODS: Diet-induced obese mouse dams were changed to standard chow during pregnancy and lactation as an intervention against predisposition for obesity and metabolic sequelea in the offspring. Expression of adipokines and TRPV4, a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis, in offspring's white adipose tissue (WAT) was assessed. RESULTS: Pathological effects on offspring's body weight, fat content, and serum insulin were fully reversed in intervention offspring on postnatal day 21. In WAT, a sixfold increase of Trpv4 mRNA expression in offspring consuming high-fat-containing diet was found, which was completely blunted in the intervention group. Simultaneously, WAT adipokine, interleukin-6, and peroxisome proliferator-activated receptor-γ mRNA and UCP1 protein expression were largely returned to control levels in intervention offspring. CONCLUSIONS: Improvement of maternal nutrition offers a powerful strategy to improve offspring's metabolic health. Targeting TRPV4-linked aspects of WAT metabolic function during early development might be a promising approach to prevent long-term adverse metabolic effects of maternal high-fat nutrition.
OBJECTIVE: One major risk factor for childhood overweight is maternal obesity. The underlying molecular mechanisms are ill-defined, and effective prevention strategies are missing. METHODS: Diet-induced obesemouse dams were changed to standard chow during pregnancy and lactation as an intervention against predisposition for obesity and metabolic sequelea in the offspring. Expression of adipokines and TRPV4, a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis, in offspring's white adipose tissue (WAT) was assessed. RESULTS: Pathological effects on offspring's body weight, fat content, and serum insulin were fully reversed in intervention offspring on postnatal day 21. In WAT, a sixfold increase of Trpv4 mRNA expression in offspring consuming high-fat-containing diet was found, which was completely blunted in the intervention group. Simultaneously, WAT adipokine, interleukin-6, and peroxisome proliferator-activated receptor-γ mRNA and UCP1 protein expression were largely returned to control levels in intervention offspring. CONCLUSIONS: Improvement of maternal nutrition offers a powerful strategy to improve offspring's metabolic health. Targeting TRPV4-linked aspects of WAT metabolic function during early development might be a promising approach to prevent long-term adverse metabolic effects of maternal high-fat nutrition.
Authors: Elena Loche; Heather L Blackmore; Asha A Carpenter; Jessica H Beeson; Adele Pinnock; Thomas J Ashmore; Catherine E Aiken; Juliana de Almeida-Faria; Josca M Schoonejans; Dino A Giussani; Denise S Fernandez-Twinn; Susan E Ozanne Journal: Cardiovasc Res Date: 2018-08-01 Impact factor: 10.787
Authors: Tobias Kretschmer; Merle Schulze-Edinghausen; Eva-Maria Turnwald; Ruth Janoschek; Inga Bae-Gartz; Peter Zentis; Marion Handwerk; Maria Wohlfarth; Astrid Schauss; Eva Hucklenbruch-Rother; Jörg Dötsch; Sarah Appel Journal: Nutrients Date: 2020-01-22 Impact factor: 5.717
Authors: Inga Bae-Gartz; Philipp Kasper; Nora Großmann; Saida Breuer; Ruth Janoschek; Tobias Kretschmer; Sarah Appel; Lisa Schmitz; Christina Vohlen; Alexander Quaas; Michal R Schweiger; Christina Grimm; Axel Fischer; Nina Ferrari; Christine Graf; Christian K Frese; Sonja Lang; Münevver Demir; Christoph Schramm; Gregor Fink; Tobias Goeser; Jörg Dötsch; Eva Hucklenbruch-Rother Journal: Sci Rep Date: 2020-09-22 Impact factor: 4.379