Obesity and Poor Healing of Wounds

A. Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.

B. Poor Healing of Wounds are defined as a condition of the inability of the body to heal the wound quickly. It may be caused by the physical state of the wound or certain health effects, such as obesity, diabetes, abnormal coagulation. etc.

C. How do calculate your BMI index
BMI= weight (kg)/ height (m2)

D. How Obesity associates with Poor Healing of Wounds
1. According to the study of "Dysfunctional γδ T Cells Contribute to Impaired Keratinocyte Homeostasis in Mouse Models of Obesity" by Taylor KR, Costanzo AE, Jameson JM. (Source from Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.,J Invest Dermatol. 2011 Aug 11. doi: 10.1038/jid.2011.241. [Epub ahead of print]), posted in PubMed,, researchers found that These studies reveal that γδ T cells are unable to regulate keratinocyte homeostasis in obesity and that the obese environment further impairs skin structure by altering cell-cell adhesion. Together, impaired keratinocyte homeostasis and epidermal barrier function through direct and indirect mechanisms result in susceptibility to skin complications, chronic wounds, and infection.

2. In a study of "Gammadelta T cells are reduced and rendered unresponsive by hyperglycemia and chronic TNFalpha in mouse models of obesity and metabolic disease" by Taylor KR, Mills RE, Costanzo AE, Jameson JM. (Source from Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, United States of America, PLoS One. 2010 Jul 2;5(7):e11422.), posted in PubMed, researchers filed in abstract that Skin gammadelta T cells that overcome this hyperglycemic state are unresponsive to epithelial cell damage due to chronic inflammatory mediators, including TNFalpha. Cytokine and growth factor production at the site of tissue damage was partially restored by administering neutralizing TNFalpha antibodies in vivo. Thus, metabolic disease negatively impacts homeostasis and functionality of skin gammadelta T cells, rendering host defense mechanisms vulnerable to injury and infection.

3. In an abstract of the study of "Wound healing in mice with high-fat diet- or ob gene-induced diabetes-obesity syndromes: a comparative study" by Seitz O, Schürmann C, Hermes N, Müller E, Pfeilschifter J, Frank S, Goren I. (Source from Pharmazentrum Frankfurt/ZAFES, Institut für Allgemeine Pharmakologie und Toxikologie, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany), posted in PubMed, researchers found that by contrast to impaired wound conditions in ob/ob mice, late wounds of HFD mice did not develop a chronic inflammatory state and were epithelialized after 11 days of repair. Thus, only genetically obese and diabetic ob/ob mice finally developed chronic wounds and therefore represent a better suited experimental model to investigate diabetes-induced wound healing disorders.

4. According to the study of "Impaired Laparotomy Wound Healing in Obese Rats" by Xing L, Culbertson EJ, Wen Y, Robson MC, Franz MG. (Source from Department of Surgery, University of Michigan, 2124F Taubman Center, 1500 East Medical Center Drive, Ann Arbor, MI, 48109-0331, USA), posted in PubMed, researchers indicated that laparotomy wound healing is impaired in obese rats. The recovery of laparotomy wound strength is delayed due to abnormal collagen maturation and remodeling, possibly due to a defect in fibroblast function. Strategies to improve outcomes for laparotomy wound healing in obese patients should include correcting the wound healing defect, possibly with growth factor or cell therapy.

5. Etc.

E. Treatments of Obesity and Poor Healing of Wounds
1. According to the abstract of the study of "Zucker diabetic fatty rat: a new model of impaired cutaneous wound repair with type II diabetes mellitus and obesity" by Slavkovsky R, Kohlerova R, Tkacova V, Jiroutova A, Tahmazoglu B, Velebny V, Rezačová M, Sobotka L, Kanta J. (Source from Laboratory of Wound Healing, CPN, Dolni Dobrouc, Czech Republic. rastik@gmail.com, Wound Repair Regen. 2011 Jul;19(4):515-25. doi: 10.1111/j.1524-475X.2011.00703.x. Epub 2011 Jun 7.), posted in PubMed, researcher indicated that The concentration of hydroxyproline in the GT of diabetic animals was significantly decreased to about one half when compared with the nondiabetic controls. The expression of interleukin-6, myeloperoxidase, stromelysin-1, and collagenase-3 was increased in the GT of diabetic rats on Day 10, while the expression of type I collagen and elastin was decreased. Taken together, Zucker diabetic fatty rats exhibited impairments in wound-size reduction, inflammatory response, tissue organization, and connective tissue turnover and are thus proposed as a new model for studying impaired repair.

2. According to the study of "Systemically and topically supplemented leptin fails to reconstitute a normal angiogenic response during skin repair in diabetic ob/ob mice" by Stallmeyer B, Pfeilschifter J, Frank S. (Source from Centre of Pharmacology, University Hospital, Johann Wolfgang Goethe University, Frankfurt am Main, Germany), posted in PubMed, researchers filed in abstracted that These data suggest that leptin reconstituted epithelial expression of VEGF during skin repair in ob/ob mice but failed to improve wound angiogenesis in the granulation tissue. Thus, the accelerated wound closure observed in leptin-supplemented ob/ob mice is not coupled to an improved wound angiogenesis.

3. Etc.

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