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The Relationship between Fat and Inflammation

Key points

  1. Fat cells are an endocrine organ which can produce inflammatory or anti-inflammatory markers.

  2. Overeating can cause fat cells to grow in size which inhibit the sugar transporter (GLUT4)

  3. Those who are overweight should consider more physical activity and less caloric intake.

  4. Cooking with natural spices is a great way to decrease inflammation.


Inflammation is a natural process which heavily influences the homeostatic balance of our tissues and organ systems. Inflammation removes pathogens and cellular material that harm our bodies.(1) As an individual’s body mass index (BMI) and body fat volume increase, macrophages begin to enter the adipose tissue and activate; behaving similar to infection.(2,3) This is mediated by NF-kB activation, which begins the pro-inflammatory cascade in the body, and leads to the downstream activation of T-helper cell 1 (TH1) and the proliferation of cytokines IL-1b, IL-6 and Tumor Necrosis Factor a (TNFa).

These markers are characterized by cellular immunity activation, and if prolonged, chronic low-grade inflammation.(2-4) An excess production of cytokines may eventually lead to tissue damage and organ system malfunction. Increases in white adipose tissue upregulate this process, and if prolonged, may lead to insulin resistance and other preventable lifestyle diseases.(1,5) The purpose of this post is to briefly explore the concomitant relationship between adiposopathy and systemic inflammation.

Overnutrition will cause an increase in visceral fat size (hypertrophy). Hypertrophic adipocytes (Fat cells) release monocyte chemoattractant protein-1 (MCP-1), a cytokine which causes chemotaxis, a process which attracts other cells. MCP-1 starts the movement of monocytes (Immune cell) into adipose tissue and initiates the differentiation from monocyte to macrophages.(5) This process changes the phenotypic expression of the adipose tissue from an M2 to an M1 state. M2 is illustrated by anti-inflammatory cytokines, IL-4, IL-10, IL-13. In contrast, M1 is characterized by proinflammatory cytokines IL-1b, IL-6 and TNFa. These pro-inflammatory mediators downregulate the GLUT4 receptor which shunts glucose to skeletal muscle and adipose tissue. Hypertrophic adipose tissue also impairs GLUT4 plasma membrane transport by essentially covering this molecule. Moreover, Macrophages and T-cells penetrate adipose tissue preventing a proper insulin response.(6-7) This process is a major contributor in insulin resistance development and eventually chronic lifestyle disease.(3-5,7)

An overabundance of glucose and fatty acids contribute towards an accumulation of macrophages in adipose tissue. The excess of nutrients regulates chemotaxis (signaling molecule) by MCP-1 and mechanisms leading to free radical proliferation and NF-kB activation which lead to inflammation and insulin resistance.(8) Lifestyle recommendations for an individual suffering from obesity-induced inflammation and insulin resistance should include a reduction in caloric intake along with an increase in activity level. (9) Obese individuals are recommended to perform resistance training rather than endurance as this will increase their metabolic rate of their skeletal muscles to a higher degree. Increased activity will reduce the number of inflammatory mediators as well as reduce the severity of insulin resistance by moving the GLUT4 receptors to the surface of the adipocyte.(7)

It is also advised to partake in an anti-inflammatory diet (no refined sugars, refined carbs or refined oils). Another good way to decrease inflammation is to increase natural spices with high levels of dietary polyphenols such as ginger, turmeric, chili powder, coriander, or rosemary which have been shown to decrease the activity of NF-kB, thus, lowering our pro-inflammatory levels. (10-12)

In conclusion, there is significant evidence to support the comorbidity of obesity, inflammation, and insulin resistance. Many chronic lifestyle diseases can be prevented by increasing our daily activity levels and by decreasing daily caloric intake which can increase insulin sensitivity. Certain spices and foods can also be included into our diets to assist in the restoration of TH2 anti-inflammatory mediators; thus, assisting our body in returning to a state of homeostatic balance, however this can be no substitute to for those who are not receiving proper activity levels or are over eating.



  1. Ellulu, MS; Patimah, I; Khaza’ai, H; Rahmat, A; Abed, Y: Obesity and inflammation: the linking mechanism and the complications. Arch Med Sci. 2017,13;4:851-863.

  2. Seaman DR; Body mass index and musculoskeletal pain: is there a connection? Chiropractic & Manual Therapies. 2013,21:15.

  3. Harford, KA; Reynolds, CM; McGillicuddy, FC; Roche, HM: Fats, inflammation and insulin resistance: insights to the role of macrophage and T-cell accumulation in adipose tissue Proceedings of the Nutrition Society. 2011,70;408–417.

  4. Esser, N; Legrand-Poels, S; Jacques, P; Scheen AJ; Paquot, N: Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes, Diabetic Research and Clinical Practice 105. 2014;141-150.

  5. Ormazabal, V; Nair, S; Elfeky, O; Aguayo, C; Salomon, C; Zuniga, FA: Association between insulin resistance and the development of cardiovascular disease, Cardiovasc Diabetol. 2018,17:122.

  6. Choe, SS; Huh, JY; Hwang, IJ; Kim, JB: Adipose Tissue Remodeling: its Role in energy Metabolism and Metabolic Disorders. Front. Endocrinol. 2016,7:30.

  7. Kim, JI; Huh, JY; Sohn, JH; Choe, SS; Lee, YS; Lim, CY; Jo, A; Park, SB; Han, W; Kim, JB: Lipid-overloaded enlarged adipocytes provoke insulin resistance independent of inflammation. Mol Cell Biol. 2015,35:1686–1699.

  8. Sell, H; Eckel, J: Adipose Tissue Inflammation: Novel Insight into the role of macrophages and lymphocytes. Current Opinion in Clinical Nutrition and Metabolic Care. 2010,13:366–370

  9. Antiainen, JP; Walker, S; Silvennoinen, M; Kyrolainen, H; Nindl, BC; Hakkinen, K; Nyman, K; Selanne, H; Hulmi, JJ: Exercise type and volume alter signaling pathways regulating skeletal muscle glucose uptake and protein synthesis. Eur J Appl Physiol. 2015,115:1835–1845

  10. Aggarwal, BB; Shishodia, S; Suppression of the Nuclear Factor-κB Activation Pathway by Spice-Derived Phytochemicals: Reasoning for Seasoning. Annals of the New York Academy of Sciences. 2004,1030(1),434–441.

  11. Agarwal, AK: Spice Up Your Life: Adipose Tissue and Inflammation. Journal of Lipids. 2014.

  12. Opara, EI; Chohan, M: Culinary Herbs and Spices: Their Bioactive Properties, the Contribution of Polyphenols and the Challenges in Deducing Their True Health Benefits. Int. J. Mol. Sci. 2014,15; 19183-19202

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