@article{OseiBlockWippert2022,
  author    = {Osei, Francis and Block, Andrea and Wippert, Pia-Maria},
  title     = {Association of primary allostatic load mediators and metabolic syndrome (MetS): A systematic review},
  series = {Frontiers in Endocrinology},
  volume    = {13},
  journal   = {Frontiers in Endocrinology},
  publisher = {Frontiers},
  address   = {Lausanne, Schweiz},
  issn      = {1664-2392},
  doi       = {10.3389/fendo.2022.946740},
  pages     = {16},
  year      = {2022},
  abstract  = {Allostatic load (AL) exposure may cause detrimental effects on the neuroendocrine system, leading to metabolic syndrome (MetS). The primary mediators of AL involve serum dehydroepiandrosterone sulfate (DHEAS; a functional HPA axis antagonist); further, cortisol, urinary norepinephrine (NE), and epinephrine (EPI) excretion levels (assessed within 12-h urine as a golden standard for the evaluation of the HPA axis activity and sympathetic nervous system activity). However, the evidence of an association between the primary mediators of AL and MetS is limited. This systematic review aimed to critically examine the association between the primary mediators of AL and MetS. PubMed and Web of Science were searched for articles from January 2010 to December 2021, published in English. The search strategy focused on cross-sectional and case-control studies comprising adult participants with MetS, obesity, overweight, and without chronic diseases. The STROBE checklist was used to assess study quality control. Of 770 studies, twenty-one studies with a total sample size (n = 10,666) met the eligibility criteria. Eighteen studies were cross-sectional, and three were case-control studies. The included studies had a completeness of reporting score of COR \% = 87.0 ± 6.4\%. It is to be noted, that cortisol as a primary mediator of AL showed an association with MetS in 50\% (urinary cortisol), 40\% (serum cortisol), 60\% (salivary cortisol), and 100\% (hair cortisol) of the studies. For DHEAS, it is to conclude that 60\% of the studies showed an association with MetS. In contrast, urinary EPI and urinary NE had 100\% no association with MetS. In summary, there is a tendency for the association between higher serum cortisol, salivary cortisol, urinary cortisol, hair cortisol, and lower levels of DHEAS with MetS. Future studies focusing on longitudinal data are warranted for clarification and understanding of the association between the primary mediators of AL and MetS.},
  language  = {en}
}
@article{BuchmannFielitzSpiraetal.2022,
  author    = {Buchmann, Nikolaus and Fielitz, Jens and Spira, Dominik and K{\"o}nig, Maximilian and Norman, Kristina and Pawelec, Graham and Goldeck, David and Demuth, Ilja and Steinhagen-Thiessen, Elisabeth},
  title     = {Muscle mass and inflammation in older adults: impact of the metabolic syndrome},
  series = {Gerontology},
  volume    = {68},
  journal   = {Gerontology},
  number    = {9},
  publisher = {Karger},
  address   = {Basel},
  issn      = {0304-324X},
  doi       = {10.1159/000520096},
  pages     = {989 -- 998},
  year      = {2022},
  abstract  = {Background: Inflammatory processes are a cause of accelerated loss of muscle mass. Metabolic syndrome (MetS) is a highly prevalent age-related condition, which may promote and be promoted by inflammation. However, whether inflammation in MetS (metaflammation) is associated with lower muscle mass is still unclear. Methods: Complete cross-sectional data on body composition, MetS, and the inflammatory markers interleukin (IL)-1 beta, IL-6, IL-10, tumor necrosis factor (TNF), and C-reactive protein (CRP) were available for 1,377 BASE-II participants (51.1\% women; 68 +/- 4 years old). Appendicular lean mass (ALM) was assessed by dual-energy X-ray absorptiometry. Low muscle mass (low ALM-to-BMI ratio [ALMBMI]) was defined according to the Foundation for the National Institutes of Health (FNIH) Sarcopenia Project. Regression models, adjusted for an increasing number of confounders (sex, age, physical activity, morbidities, diabetes mellitus type II, TSH, albumin, HbA1c, smoking habits, alcohol intake, education, and energy intake/day), were used to calculate the association between low ALMBMI and high inflammation (tertile 3) according to MetS. Results: MetS was present in 36.2\% of the study population, and 9\% had low ALMBMI. In the whole study population, high CRP (odds ratio [OR]: 2.7 [95\% CI: 1.6-4.7; p = 0.001]) and high IL-6 (OR: 2.1 [95\% CI: 1.2-1.9; p = 0.005]) were associated with low ALMBMI. In contrast, no significant association was found between TNF, IL-10, or IL-1 beta with low ALMBMI. When participants were stratified by MetS, results for IL-6 remained significant only in participants with MetS. Conclusions: Among BASE-II participants, low ALMBMI was associated with inflammation. Low-grade inflammation triggered by disease state, especially in the context of MetS, might favor loss of muscle mass, so a better control of MetS might help to prevent sarcopenia. Intervention studies to test whether strategies to prevent MetS might also prevent loss of muscle mass seem to be promising.},
  language  = {en}
}
@article{KaruwanarintPhonratTungtrongchitretal.2018,
  author    = {Karuwanarint, Piyaporn and Phonrat, Benjaluck and Tungtrongchitr, Anchalee and Suriyaprom, Kanjana and Chuengsamarn, Somlak and Schweigert, Florian J. and Tungtrongchitr, Rungsunn},
  title     = {Vitamin D-binding protein and its polymorphisms as a predictor for metabolic syndrome},
  series = {Biomarkers in medicine},
  volume    = {12},
  journal   = {Biomarkers in medicine},
  number    = {5},
  publisher = {Future Medicine},
  address   = {London},
  issn      = {1752-0363},
  doi       = {10.2217/bmm-2018-0029},
  pages     = {465 -- 473},
  year      = {2018},
  abstract  = {Aim: To investigate the relationship of vitamin D-binding protein (GC) and genetic variation of GC (rs4588, rs7041 and rs2282679) with metabolic syndrome (MetS) in the Thai population. Materials \& methods: GCglobulin concentrations were measured by quantitative western blot analysis in 401 adults. All participants were genotyped using TaqMan allelic discrimination assays. Results: GC-globulin levels were significatly lower in MetS subjects than in control subjects, in which significant negative correlations of GC-globulin levels with systolic blood pressure, glucose and age were found. Male participants who carried the GT genotype for rs4588 showed an increased risk of MetS compared with the GG wild-type (odds ratio: 3.25; p = 0.004). Conclusion: GC-globulin concentrations and variation in GC rs4588 were supported as a risk factor for MetS in Thais.},
  language  = {en}
}
@article{ManowskyCamargoKippetal.2016,
  author    = {Manowsky, Julia and Camargo, Rodolfo Gonzalez and Kipp, Anna Patricia and Henkel, Janin and P{\"u}schel, Gerhard Paul},
  title     = {Insulin-induced cytokine production in macrophages causes insulin resistance in hepatocytes},
  series = {American journal of physiology : Endocrinology and metabolism},
  volume    = {310},
  journal   = {American journal of physiology : Endocrinology and metabolism},
  publisher = {American Chemical Society},
  address   = {Bethesda},
  issn      = {0193-1849},
  doi       = {10.1152/ajpendo.00427.2015},
  pages     = {E938 -- E946},
  year      = {2016},
  abstract  = {Overweight and obesity are associated with hyperinsulinemia, insulin resistance, and a low-grade inflammation. Although hyperinsulinemia is generally thought to result from an attempt of the beta-cell to compensate for insulin resistance, there is evidence that hyperinsulinaemia itself may contribute to the development of insulin resistance and possibly the low-grade inflammation. To test this hypothesis, U937 macrophages were exposed to insulin. In these cells, insulin induced expression of the proinflammatory cytokines IL-1 beta, IL-8, CCL2, and OSM. The insulin-elicited induction of IL-1 beta was independent of the presence of endotoxin and most likely mediated by an insulin-dependent activation of NF-kappa B. Supernatants of the insulin-treated U937 macrophages rendered primary cultures of rat hepatocytes insulin resistant; they attenuated the insulin-dependent induction of glucokinase by 50\%. The cytokines contained in the supernatants of insulin-treated U937 macrophages activated ERK1/2 and IKK beta, resulting in an inhibitory serine phosphorylation of the insulin receptor substrate. In addition, STAT3 was activated and SOCS3 induced, further contributing to the interruption of the insulin receptor signal chain in hepatocytes. These results indicate that hyperinsulinemia per se might contribute to the low-grade inflammation prevailing in overweight and obese patients and thereby promote the development of insulin resistance particularly in the liver, because the insulin concentration in the portal circulation is much higher than in all other tissues.},
  language  = {en}
}