Table 2.
Summary of Obese animal models publish manuscripts.
| Reference Paper | Title | Study Design | Major Finding |
|---|---|---|---|
| Wernstedt 2014, [27] | Adipocyte inflammation is essential for healthy adipose tissue expansion and remodeling | Three mouse models with adipose tissue | High fat diet expands the adipocyte, increases hepatic steatosis and metabolic dysfunction. |
| Wu 2011, [28] | Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis | White adipose tissue analyzed from mice model | Mice on high fat diet develop increased body fat, impaired glucose tolerance and insulin resistance in the absence of eosinophils. |
| Feuerer 2009, [29] | Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters | Mice model highly enriched in abdominal fat | Loss of function and gain of function experiments revealed that T (reg) cells influence inflammatory state of adipose tissue and thus insulin resistance. |
| Hotamisligil 1993, [30] | Adipose expression of tumor necrosis factor-α direct role in obesity-linked insulin resistance | Mouse models with induced high fat diet | TNF-α RNA expression was observed from four different rodent models |
| Uysal 1997, [31] | Protection from obesity-induced insulin resistance in mice lacking TNF-α function | Obese mice with a targeted null mutation in the gene encoding TNF-α | The absence of TNF-α resulted in significantly improved insulin sensitivity in diet induced mice obesity. |
| Arai S 2013, [32] | Obesity-associated autoantibody production requires AIM to retain the immunoglobulin M immune complex on follicular dendritic cells | Obese mouse model AIM (apoptosis inhibitor macrophages) deficient | IgM-AIM association contributes to autoantibody production under obese conditions |
| LEE 2014, [33] | Increased adipocyte O2 consumption triggers HIF-1alpha, causing inflammation and insulin resistance in obesity | Obese mouse model | early in the course of high-fat diet (HFD) feeding and obesity, adipocyte respiration becomes uncoupled, leading to increased oxygen consumption and a state of relative adipocyte hypoxia |