Acute hyperinsulinemia raises plasma interleukin-6 in both nondiabetic and type 2 diabetes mellitus subjects, and this effect is inversely associated with body mass index

Ruge, Toralph; Lockton, J. A.; Renström, Frida; Lystig, Theodore C.; Sukonina, Valentina; Svensson, Maria; Eriksson, Jan W.

doi:10.1016/j.metabol.2009.02.010

Cited by 58 publications

(36 citation statements)

References 32 publications

(43 reference statements)

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“…The increase in whole body glucose disposal rate (M) did not reach significance (P ϭ 0.1); this might have been influenced by the number of subjects in this study; moreover, it is to be noted that the response of glucose disposal rate to the hypocaloric diet is variable and some studies report no increase during the diet (12,13,25). The findings in our prospective study are in line with results of the cross-sectional study of Ruge et al (24). They found a higher responsiveness of plasma IL-6 to hyperinsulinemia in healthy lean subjects compared with insulin-resistant subjects.…”

Section: Discussionsupporting

confidence: 83%

Effect of hyperinsulinemia and very-low-calorie diet on interstitial cytokine levels in subcutaneous adipose tissue of obese women

Šiklová

Polàk

Klimčáková

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Hyperinsulinemia, frequently present in type 2 diabetes and obesity, might be one of the drivers of the enhanced production of adipocytokines. The aim of this study was to investigate the interstitial levels of cytokines in subcutaneous adipose tissue (SCAT) in response to hyperinsulinemia and the effect of weightreducing hypocaloric diet on this regulation in obese subjects. Thirteen obese premenopausal women participated in the study. Concentrations of seven cytokines were measured in plasma and in AT interstitial fluid collected by microdialysis during a euglycemichyperinsulinemic clamp and during control infusion of physiological saline. A subgroup of six women underwent a 4-wk very-low-calorie diet (VLCD). Microdialysis during the clamp was performed before and at the end of VLCD. Hyperinsulinemia induced an increase of monocyte chemoatractant protein (MCP-1) and IL-6 SCAT interstitial and plasma levels and elevated IL-8 levels in SCAT. The relative changes of IL-6 levels in the dialysate correlated with changes of IL-8 and MCP-1. The interstitial and plasma levels of IL-1␤, IL-10, TNF␣, and plasminogen activator inhibitor (PAI-1) remained unchanged in response to hyperinsulinemia. VLCD resulted in enhancement of the hyperinsulinemia-induced augmentation of MCP-1, IL-6, and IL-8 interstitial levels. In conclusion, hyperinsulinemia upregulates the interstitial levels of MCP-1, IL-6, and IL-8 in SCAT in obese women, whereas it does not affect IL-1␤, IL-10, TNF␣, and PAI-1 levels. Hypocaloric diet associated with weight reduction enhances the hyperinsulinemia-induced upregulation of MCP-1, IL-6, and IL-8 in SCAT. microdialysis; adipose tissue; adipokines ADIPOSE TISSUE (AT) is an active endocrine organ that releases a large number of cytokines and bioactive mediators, called adipokines. In obese and type 2 diabetic subjects, production of many AT-derived substances is increased, associating obesity with a low-grade inflammation state (2-4, 11). Cytokines and chemokines secreted from AT have also been suggested to be among factors that are responsible for the development of insulin resistance (IR) (14,36). Relationships between cytokines and insulin signaling pathways have been observed in several studies (23,26,28,30). Monocyte chemoattractant protein-1 (MCP-1) impairs insulin signaling in skeletal muscle cells at doses similar to its physiological plasma concentrations (ϳ200 pg/ml)(26). Tumor necrosis factor-␣ (TNF␣) interferes directly with the insulin signaling cascade in human adipocytes, decreasing insulin-induced glucose uptake through downregulation of PI 3-kinase (19). In 3T3-L1 adipocytes, interleukin-1␤ (IL-1␤), IL-6, and TNF␣ deteriorate insulin signaling pathways via downregulation of IRS-1 and GLUT4 expression (23,28,30).The primary cause of increased levels of circulating adipokines in obesity is unknown. In obese prediabetic patients, before hyperglycemia is developed, chronic hyperinsulinemia is observed, often associated with increased IL-8, TNF␣, and IL-6 circulating levels (2, 3, 11). Theref...

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Section: Discussionsupporting

confidence: 83%

Effect of hyperinsulinemia and very-low-calorie diet on interstitial cytokine levels in subcutaneous adipose tissue of obese women

Šiklová

Polàk

Klimčáková

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Free fatty acids are also implicated in inflammation and insulin resistance, as described later in this review. While hyperglycaemia can induce oxidative stress (Dandona et al 2007), studies have shown that acute hyperglycaemia can increase pro-inflammatory adipokines such as IL6 and TNFa levels in non-diabetic as well as IGT subjects (Esposito et al 2002) and IL6 in non-diabetic and T2DM subjects (Ruge et al 2009). …”

Section: The Effect Of Glucose On Adipokine Inflammationmentioning

confidence: 99%

Adipokine inflammation and insulin resistance: the role of glucose, lipids and endotoxin

Piya¹,

McTernan²,

Kumar³

2012

Journal of Endocrinology

220

165

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Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multifunctional secretory organ with the capacity to control energy homoeostasis through peripheral and central regulation of energy homoeostasis. It also plays an important role in innate immunity. However, the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low-grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or LPS. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, how nutrients such as these can influence adipokine inflammation and consequently insulin resistance directly through their effects on secretion of adipocytokines (TNFa, IL6 and resistin) as well as indirectly through increases in endotoxin is discussed.

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“…Hyperinsulinemia has been shown to increase both tumor necrosis factor-a (TNF-a) mRNA in adipose tissue (Krogh-Madsen et al, 2004) and TNF-a concentrations in plasma (Ruge et al, 2009). Interactions between inflammation and metabolic dysregulation are, however, largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Postprandial hyperglycemia and insulin response are affected by sea buckthorn (Hippophaë rhamnoides ssp. turkestanica) berry and its ethanol-soluble metabolites

Järvinen

Linderborg

et al. 2010

Eur J Clin Nutr

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Background/Objectives: Repeated postprandial hyperglycemia and subsequent mild, late hypoglycemia as well as high postprandial insulin response lead to metabolic events that may eventually develop into type 2 diabetes. The aim of this study was to assess how sea buckthorn berries as well as two sea buckthorn extraction residues modulate the postprandial metabolism after a high-glucose meal. Subjects/Methods: Ten healthy normal-weight male volunteers consumed four study breakfasts, one control (A) and three sea buckthorn meals on four distinct study days. All the meals contained yoghurt and glucose (50 g). The sea buckthorn ingredients used were dried and crushed whole berries (meal B1), supercritical fluid (SF)-carbon dioxide (CO 2 )-extracted oil-free berries (meal B2) or ethanol-extracted SF-CO 2 -extraction residue (meal B3). Blood samples for glucose, insulin and tumor necrosis factor-a analyses were collected before and during the 6-h study period. Results: Meal B1 suppressed the postprandial peak insulin response when compared with meal A (Dconcentration of 30-min peak value À21.8 mU/l, P ¼ 0.039), and stabilized postprandial hyperglycemia and subsequent hypoglycemia (Dconcentration of 30-min peak value-120-min value À30.4 mU/l, P ¼ 0.036). Furthermore, meal B2 resulted in a more stable insulin response than the control meal (Dconcentration of 30-min peak value-120-min value À25.9 mU/l, P ¼ 0.037). Conclusions: Removal of the CO 2 -soluble oil component from the berries did not show a significant change in the studied postprandial effects of the berries. The EtOH soluble components, again showed advantageous properties in both insulin and glucose responses.

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Acute hyperinsulinemia raises plasma interleukin-6 in both nondiabetic and type 2 diabetes mellitus subjects, and this effect is inversely associated with body mass index

Cited by 58 publications

References 32 publications

Effect of hyperinsulinemia and very-low-calorie diet on interstitial cytokine levels in subcutaneous adipose tissue of obese women

Effect of hyperinsulinemia and very-low-calorie diet on interstitial cytokine levels in subcutaneous adipose tissue of obese women

Adipokine inflammation and insulin resistance: the role of glucose, lipids and endotoxin

Postprandial hyperglycemia and insulin response are affected by sea buckthorn (Hippophaë rhamnoides ssp. turkestanica) berry and its ethanol-soluble metabolites

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