@article{GohlkeManciniGarciaCarrizoetal.2021,
  author    = {Gohlke, Sabrina and Mancini, Carola and Garcia-Carrizo, Francisco and Schulz, Tim J.},
  title     = {Loss of the ciliary gene Bbs4 results in defective thermogenesis due to metabolic inefficiency and impaired lipid metabolism},
  series = {The FASEB journal : the official journal of the Federation of American Societies for Experimental Biology},
  volume    = {35},
  journal   = {The FASEB journal : the official journal of the Federation of American Societies for Experimental Biology},
  number    = {11},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {1530-6860},
  doi       = {10.1096/fj.202100772RR},
  pages     = {13},
  year      = {2021},
  abstract  = {Adipose tissue is central to the regulation of energy balance. While white adipose tissue (WAT) is responsible for triglyceride storage, brown adipose tissue specializes in energy expenditure. Deterioration of brown adipocyte function contributes to the development of metabolic complications like obesity and diabetes. These disorders are also leading symptoms of the Bardet-Biedl syndrome (BBS), a hereditary disorder in humans which is caused by dysfunctions of the primary cilium and which therefore belongs to the group of ciliopathies. The cilium is a hair-like organelle involved in cellular signal transduction. The BBSome, a supercomplex of several Bbs gene products, localizes to the basal body of cilia and is thought to be involved in protein sorting to and from the ciliary membrane. The effects of a functional BBSome on energy metabolism and lipid mobilization in brown and white adipocytes were tested in whole-body Bbs4 knockout mice that were subjected to metabolic challenges. Chronic cold exposure reveals cold-intolerance of knockout mice but also ameliorates the markers of metabolic pathology detected in knockouts prior to cold. Hepatic triglyceride content is markedly reduced in knockout mice while circulating lipids are elevated, altogether suggesting that defective lipid metabolism in adipose tissue creates increased demand for systemic lipid mobilization to meet energetic demands of reduced body temperatures. These findings taken together suggest that Bbs4 is essential for the regulation of adipose tissue lipid metabolism, representing a potential target to treat metabolic disorders.},
  language  = {en}
}
@article{HauffeRathAgyapongetal.2022,
  author    = {Hauffe, Robert and Rath, Michaela and Agyapong, Wilson and Jonas, Wenke and Vogel, Heike and Schulz, Tim Julius and Schwarz, Maria and Kipp, Anna Patricia and Bl{\"u}her, Matthias and Kleinridders, Andr{\´e}},
  title     = {Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling},
  series = {Antioxidants},
  volume    = {11},
  journal   = {Antioxidants},
  edition   = {5},
  publisher = {MDPI},
  address   = {Basel, Schweiz},
  issn      = {2076-3921},
  doi       = {10.3390/antiox11050862},
  pages     = {1 -- 16},
  year      = {2022},
  abstract  = {The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can protect against the development of diet-induced insulin resistance in white adipose tissue (WAT) by increasing glutathione peroxidase 3 (GPx3) and insulin receptor (IR) expression. Whether selenite (Se) can attenuate insulin resistance in established lipotoxic and obese conditions is unclear. We confirm that GPX3 mRNA expression in adipose tissue correlates with BMI in humans. Cultivating 3T3-L1 pre-adipocytes in palmitate-containing medium followed by Se treatment attenuates insulin resistance with enhanced GPx3 and IR expression and adipocyte differentiation. However, feeding obese mice a selenium-enriched high-fat diet (SRHFD) only resulted in a modest increase in overall selenoprotein gene expression in WAT in mice with unaltered body weight development, glucose tolerance, and insulin resistance. While Se supplementation improved adipocyte morphology, it did not alter WAT insulin sensitivity. However, mice fed a SRHFD exhibited increased insulin content in the pancreas. Overall, while selenite protects against palmitate-induced insulin resistance in vitro, obesity impedes the effect of selenite on insulin action and adipose tissue metabolism in vivo.},
  language  = {en}
}
@article{MusalekKokstejnPapezetal.2017,
  author    = {Musalek, Martin and Kokstejn, Jakub and Papez, Pavel and Scheffler, Christiane and Mumm, Rebekka and Czernitzki, Anna-Franziska and Koziel, Slawomir},
  title     = {Impact of normal weight obesity on fundamental motor skills in pre-school children aged 3 to 6 years},
  series = {Journal of biological and clinical anthropology : Anthropologischer Anzeiger ; Mitteilungsorgan der Gesellschaft f{\"u}r Anthropologie},
  volume    = {74},
  journal   = {Journal of biological and clinical anthropology : Anthropologischer Anzeiger ; Mitteilungsorgan der Gesellschaft f{\"u}r Anthropologie},
  publisher = {Schweizerbart},
  address   = {Stuttgart},
  issn      = {0003-5548},
  doi       = {10.1127/anthranz/2017/0752},
  pages     = {203 -- 212},
  year      = {2017},
  abstract  = {Normal weight obesity is defined as having excessive body fat, but normal BMI. Even though previous research revealed that excessive body fat in children inhibited their physical activity and decreased motor performance, there has been only little evidence about motor performance of normal weight obese children. This study aims to establish whether normal weight obese pre-school children aged 3-6 years will have a significantly worse level of fundamental motor skills compared to normal weight non-obese counterparts. The research sample consisted of 152 pre-schoolers selected from a specific district of Prague, the Czech Republic. According to values from four skinfolds: triceps, subscapula, suprailiaca, calf, and BMI three categories of children aged 3-6 years were determined: A) normal weight obese n = 51; B) normal weight non-obese n = 52; C) overweight and obese n = 49. The Movement Assessment Battery for Children (MABC-2) was used for the assessment of fundamental motor skills. Normal weight obese children had significantly higher amount of adipose tissue p < 0.001 than normal weight non-obese children but the same average BMI. Moreover, normal weight obese children did not have significantly less amount of subcutaneous fat on triceps and calf compared to their overweight and obese peers. In majority of MABC-2 tests, normal weight obese pre-schoolers showed the poorest performance. Moreover, normal weight obese children had significantly worse total standard score = 38.82 compared to normal weight non-obese peers = 52.27; p < 0.05. In addition, normal weight obese children had a more than three times higher frequency OR = 3.69 CI95\% (1.10; 12.35) of severe motor deficit performance <= 5th centile of the MABC-2 norm. These findings are strongly alarming since indices like BMI are not able to identify normal weight obese individual. We recommend verifying real portion of normal weight obese children as they are probably in higher risk of health and motor problems than overweight and obese population due to their low lean mass.},
  language  = {en}
}
@article{GrajaGarciaCarrizoJanketal.2018,
  author    = {Graja, Antonia and Garcia-Carrizo, Francisco and Jank, Anne-Marie and Gohlke, Sabrina and Ambrosi, Thomas H. and Jonas, Wenke and Ussar, Siegfried and Kern, Matthias and Sch{\"u}rmann, Annette and Aleksandrova, Krasimira and Bluher, Matthias and Schulz, Tim Julius},
  title     = {Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism},
  series = {Aging Cell},
  volume    = {17},
  journal   = {Aging Cell},
  number    = {5},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {1474-9718},
  doi       = {10.1111/acel.12810},
  pages     = {13},
  year      = {2018},
  abstract  = {Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well-known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue-resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix-modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue-resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high-fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age-related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age-related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.},
  language  = {en}
}