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Short-term overfeeding may induce peripheral insulin resistance without altering subcutaneous adipose tissue macrophages in humans.

Tam CS, Viardot A, Clément K, Tordjman J, Tonks K, Greenfield JR, Campbell LV, Samocha-Bonet D, Heilbronn LK - Diabetes (2010)

Bottom Line: Insulin sensitivity decreased by 11% from 54.6 +/- 18.7 to 48.9 +/- 15.7 micromol/(kg of FFM)/min (P = 0.01).There was a significant increase in circulating C-reactive protein (P = 0.002) and monocyte chemoattractant protein-1 (P = 0.01), but no change in interleukin-6 and intercellular adhesion molecule-1.There were no changes in fat cell size, the number of adipose tissue macrophages or T-cells, or inflammatory gene expression and no change in circulating immune cell number or expression of their surface activation markers after overfeeding.

View Article: PubMed Central - PubMed

Affiliation: Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia.

ABSTRACT

Objective: Chronic low-grade inflammation is a feature of obesity and is postulated to be causal in the development of insulin resistance and type 2 diabetes. The aim of this study was to assess whether overfeeding induces peripheral insulin resistance in lean and overweight humans, and, if so, whether it is associated with increased systemic and adipose tissue inflammation.

Research design and methods: Thirty-six healthy individuals undertook 28 days of overfeeding by +1,250 kcal/day (45% fat). Weight, body composition, insulin sensitivity (hyperinsulinemic-euglycemic clamp), serum and gene expression of inflammation markers, immune cell activation, fat cell size, macrophage and T-cell numbers in abdominal subcutaneous adipose tissue (flow cytometry and immunohistochemistry) were assessed at baseline and after 28 days.

Results: Subjects gained 2.7 +/- 1.6 kg (P < 0.001) and increased fat mass by 1.1 +/- 1.6% (P < 0.001). Insulin sensitivity decreased by 11% from 54.6 +/- 18.7 to 48.9 +/- 15.7 micromol/(kg of FFM)/min (P = 0.01). There was a significant increase in circulating C-reactive protein (P = 0.002) and monocyte chemoattractant protein-1 (P = 0.01), but no change in interleukin-6 and intercellular adhesion molecule-1. There were no changes in fat cell size, the number of adipose tissue macrophages or T-cells, or inflammatory gene expression and no change in circulating immune cell number or expression of their surface activation markers after overfeeding.

Conclusions: Weight gain-induced insulin resistance was observed in the absence of a significant inflammatory state, suggesting that inflammation in subcutaneous adipose tissue occurs subsequent to peripheral insulin resistance in humans.

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Related in: MedlinePlus

Circulating immune cell numbers. Relative cell numbers of circulating immune cell subsets, expressed as a percentage of total white blood cells [granulocytes (G), monocytes (M), lymphocytes (L), or T-cells (T)] or as a percentage of T-lymphocytes (CD4, CD8) or as a percentage of CD4+ T-cells [T-helper cells type 1 (Th1) and type 2 (Th2)] at baseline (black bars) and after 28 days of overfeeding (open bars). Data are presented as means ± SEM.
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Figure 4: Circulating immune cell numbers. Relative cell numbers of circulating immune cell subsets, expressed as a percentage of total white blood cells [granulocytes (G), monocytes (M), lymphocytes (L), or T-cells (T)] or as a percentage of T-lymphocytes (CD4, CD8) or as a percentage of CD4+ T-cells [T-helper cells type 1 (Th1) and type 2 (Th2)] at baseline (black bars) and after 28 days of overfeeding (open bars). Data are presented as means ± SEM.

Mentions: Circulating immune cells were also analyzed by flow cytometry at both visits, with a focus on cell numbers of major immune cell subsets and on expression of cell surface activation markers on different subsets. There was no change in relative cell number of neutrophils, monocytes, and lymphocytes after 28 days of overfeeding (Fig. 4). Similarly, numbers of CD4+ T-helper cells, including the specific phenotypes type 1 and type 2, as well as CD8+ cytotoxic T-cells, did not change over the 28-day overfeeding period. Furthermore, expression of activation markers CD66b, CD62L, and CD11b on neutrophils and monocytes, as well as CD69, CD62L, and CD25 on T-cells were not changed by overfeeding (Table 2).


Short-term overfeeding may induce peripheral insulin resistance without altering subcutaneous adipose tissue macrophages in humans.

Tam CS, Viardot A, Clément K, Tordjman J, Tonks K, Greenfield JR, Campbell LV, Samocha-Bonet D, Heilbronn LK - Diabetes (2010)

Circulating immune cell numbers. Relative cell numbers of circulating immune cell subsets, expressed as a percentage of total white blood cells [granulocytes (G), monocytes (M), lymphocytes (L), or T-cells (T)] or as a percentage of T-lymphocytes (CD4, CD8) or as a percentage of CD4+ T-cells [T-helper cells type 1 (Th1) and type 2 (Th2)] at baseline (black bars) and after 28 days of overfeeding (open bars). Data are presented as means ± SEM.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2927938&req=5

Figure 4: Circulating immune cell numbers. Relative cell numbers of circulating immune cell subsets, expressed as a percentage of total white blood cells [granulocytes (G), monocytes (M), lymphocytes (L), or T-cells (T)] or as a percentage of T-lymphocytes (CD4, CD8) or as a percentage of CD4+ T-cells [T-helper cells type 1 (Th1) and type 2 (Th2)] at baseline (black bars) and after 28 days of overfeeding (open bars). Data are presented as means ± SEM.
Mentions: Circulating immune cells were also analyzed by flow cytometry at both visits, with a focus on cell numbers of major immune cell subsets and on expression of cell surface activation markers on different subsets. There was no change in relative cell number of neutrophils, monocytes, and lymphocytes after 28 days of overfeeding (Fig. 4). Similarly, numbers of CD4+ T-helper cells, including the specific phenotypes type 1 and type 2, as well as CD8+ cytotoxic T-cells, did not change over the 28-day overfeeding period. Furthermore, expression of activation markers CD66b, CD62L, and CD11b on neutrophils and monocytes, as well as CD69, CD62L, and CD25 on T-cells were not changed by overfeeding (Table 2).

Bottom Line: Insulin sensitivity decreased by 11% from 54.6 +/- 18.7 to 48.9 +/- 15.7 micromol/(kg of FFM)/min (P = 0.01).There was a significant increase in circulating C-reactive protein (P = 0.002) and monocyte chemoattractant protein-1 (P = 0.01), but no change in interleukin-6 and intercellular adhesion molecule-1.There were no changes in fat cell size, the number of adipose tissue macrophages or T-cells, or inflammatory gene expression and no change in circulating immune cell number or expression of their surface activation markers after overfeeding.

View Article: PubMed Central - PubMed

Affiliation: Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia.

ABSTRACT

Objective: Chronic low-grade inflammation is a feature of obesity and is postulated to be causal in the development of insulin resistance and type 2 diabetes. The aim of this study was to assess whether overfeeding induces peripheral insulin resistance in lean and overweight humans, and, if so, whether it is associated with increased systemic and adipose tissue inflammation.

Research design and methods: Thirty-six healthy individuals undertook 28 days of overfeeding by +1,250 kcal/day (45% fat). Weight, body composition, insulin sensitivity (hyperinsulinemic-euglycemic clamp), serum and gene expression of inflammation markers, immune cell activation, fat cell size, macrophage and T-cell numbers in abdominal subcutaneous adipose tissue (flow cytometry and immunohistochemistry) were assessed at baseline and after 28 days.

Results: Subjects gained 2.7 +/- 1.6 kg (P < 0.001) and increased fat mass by 1.1 +/- 1.6% (P < 0.001). Insulin sensitivity decreased by 11% from 54.6 +/- 18.7 to 48.9 +/- 15.7 micromol/(kg of FFM)/min (P = 0.01). There was a significant increase in circulating C-reactive protein (P = 0.002) and monocyte chemoattractant protein-1 (P = 0.01), but no change in interleukin-6 and intercellular adhesion molecule-1. There were no changes in fat cell size, the number of adipose tissue macrophages or T-cells, or inflammatory gene expression and no change in circulating immune cell number or expression of their surface activation markers after overfeeding.

Conclusions: Weight gain-induced insulin resistance was observed in the absence of a significant inflammatory state, suggesting that inflammation in subcutaneous adipose tissue occurs subsequent to peripheral insulin resistance in humans.

Show MeSH
Related in: MedlinePlus