Oral Presentation The Annual Scientific Meeting of the Australian Diabetes Society and the Australian Diabetes Educators Association 2013

Adipose tissue regulation of cell-mediated inflammation and 12-month outcomes after bariatric surgery in obesity and type 2 diabetes. (#156)

Katherine Samaras 1 2 , Elizabeth Blanchard 1 , Reginald V N Lord 3 4
  1. Diabetes and Metabolism Division, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia
  2. Department of Endocrinology, St Vincent’s Hospital, Darlinghurst, NSW, Australia
  3. St. Vincent’s Centre for Applied Medical Research, University of NSW, Darlinghurst, NSW, Australia
  4. . Department of Upper Gastrointestinal Surgery, St Vincent’s Hospital, Darlinghurst, NSW, Australia

Low-grade inflammation characterizes obesity-associated type 2 diabetes mellitus. We have previously shown that greater reductions in circulating pro-inflammatory lymphocytes after bariatric surgery is closely associated with greater reductions in glucose in obese humans with type 2 diabetes. To further interrogate the nexus between cell-mediated immunity and weight and glycaemic responses, we examined adipose tissue gene expression of cytokines regulating systemic inflammation and responses after bariatric surgery.

Methods: Obese-subjects (n=36) undertaking gastric banding had measures of weight, HbA1c and fasting glucose at 6 and 12m. At surgery, subcutaneous (SAT) and visceral adipose tissue were collected and gene expression undertaken of molecules regulating inflammation. Adipose tissue gene expression data were analyzed against the 6 and 12m changes in weight, glucose and HbA1c.

Results- Weight loss and glucose responses after bariatric surgery are shown below.

N=36

Baseline (mean±SD)

12 months (mean±SD)

Age (years)

50.3±12.3

Weight (kg)

118.5±22.0

101.6 ±18.4†

BMI (kg/m2)

41.6±5.9

35.8 ±5.3†

Waist (cm)

122 17

112±16†

F glucose (mmol/L)

7.2±2.2

5.5±1.5†

HbA1c (n=17)

7.0±1.7

6.6±1.2*

* Baseline vs 12n p=0.004; †p<0.0001

There were inverse associations between SAT gene expression of molecules promoting cell-mediated inflammation and the reduction in weight, glucose and HbA1c after bariatric surgery. ∆weight was inversely associated with expression of macrophage inflammatory protein-1 (MIP-1) (6m: ß=-0.34, p=0.017; 12m: ß=-0.33, p=0.03), and interferon-γ (6m: ß= -0.59, p=0.027; 12m: ß= -0.69, p=0.01). ∆FG was inversely associated with expression of MIP-1 (6m: ß= -0.92, p=0.002; 12m: ß= -0.86, p=0.007) and macrophage chemotactic protein-1 (MCP-1) (6m: ß= -0.69, p=0.018; 12m: ß= -0.65, p=0.039). ∆HbA1c was associated with M1P-1 expression (12m: ß= -0.88, p=0.006).

Conclusion: Lower SAT gene expression of molecules promoting cell-mediated inflammation is associated with greater reductions in weight, glucose and HbA1c after bariatric surgery. The interaction between cell-mediated immunity and glucose metabolism in obesity-associated type 2 diabetes requires further investigation for potential treatment opportunities.