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Friedline, Randall H.,Ko, Hwi Jin,Jung, Dae Young,Lee, Yongjin,Bortell, Rita,Dagdeviren, Sezin,Patel, Payal R.,Hu, Xiaodi,Inashima, Kunikazu,Kearns, Caitlyn,Tsitsilianos, Nicholas,Shafiq, Umber,Shultz The Federation of American Societies for Experimen 2016 The FASEB Journal Vol.30 No.3
<P>Obesity is characterized by a dysregulated immune system, which may causally associate with insulin resistance and type 2 diabetes. Despite widespread use of nonobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2 common chain receptor (NSG) mice as animal models of human diseases including type 1 diabetes, the underlying metabolic effects of a genetically altered immune system are poorly understood. For this, we performed a comprehensive metabolic characterization of these mice fed chow or after 6 wk of a high-fat diet. We found that NOD mice had similar to 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-euglycemic clamp, than C57BL/6 wild-type mice. SCID mice were also more insulin sensitive with increased muscle glucose metabolism and resistant to diet-induced obesity due to increased energy expenditure (similar to 10%) and physical activity (similar to 40%) as measured by metabolic cages. NSG mice were completely protected from diet-induced obesity and insulin resistance with significant increases in glucose metabolism in peripheral organs. Our findings demonstrate an important role of genetic background, lymphocytes, and cytokine signaling in diet-induced obesity and insulin resistance.</P>
I am not relieved from role strain. I've lost my job
Il Sung Nan,Terri Friedline,Ah Young Choi 한국노인복지학회 2014 International Journal of Welfare for the Aged Vol.30 No.-
This study examined the relationship of family and friends to the resiliency of older widows. Data from the National Social Life, Health, and Aging Project (NSHAP) survey (Waite et al., 2007), which sampled persons 57-85 years of age (n=3005), was used. It was hypothesized that older widows have greater breadth and depth of family and friend relationships than older married adults. Multiple regression analysis results revealed that older widows engaged more frequently in family and friend relations compared to older married adults, possibly enabling greater resilience to widowhood.
Kim, Jong Hun,Lee, Eunjung,Friedline, Randall H.,Suk, Sujin,Jung, Dae Young,Dagdeviren, Sezin,Hu, Xiaodi,Inashima, Kunikazu,Noh, Hye Lim,Kwon, Jung Yeon,Nambu, Aya,Huh, Jun R.,Han, Myoung Sook,Davis, Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.4
<P>Obesity-mediated inflammation is a major cause of insulin resistance, and macrophages play an important role in this process. The 78-kDa glucose-regulated protein (GRP78) is a major endoplasmic reticulum chaperone that modulates unfolded protein response (UPR), and mice with GRP78 heterozygosity were resistant to diet-induced obesity. Here, we show that mice with macrophage-selective ablation of GRP78 (Lyz-GRP78(-/-)) are protected from skeletal muscle insulin resistance without changes in obesity compared with wild-type mice after 9 wk of high-fat diet. GRP78-deficient macrophages demonstrated adapted UPR with up-regulation of activating transcription factor (ATF)-4 and M2-polarization markers. Diet-induced adipose tissue inflammation was reduced, and bone marrow-derived macrophages from Lyz-GRP78(-/-) mice demonstrated a selective increase in IL-6 expression. Serum IL-13 levels were elevated by >4-fold in Lyz-GRP78(-/-) mice, and IL-6 stimulated the myocyte expression of IL-13 and IL-13 receptor. Lastly, recombinant IL-13 acutely increased glucose metabolism in Lyz-GRP78(-/-) mice. Taken together, our data indicate that GRP78 deficiency activates UPR by increasing ATF-4, and promotes M2-polarization of macrophages with a selective increase in IL-6 secretion. Macrophage-derived IL-6 stimulates the myocyte expression of IL-13 and regulates muscle glucose metabolism in a paracrine manner. Thus, our findings identify a novel crosstalk between macrophages and skeletal muscle in the modulation of obesity-mediated insulin resistance.</P>
IL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle
Dagdeviren, Sezin,Jung, Dae Young,Friedline, Randall H.,Noh, Hye Lim,Kim, Jong Hun,Patel, Payal R.,Tsitsilianos, Nicholas,Inashima, Kunikazu,Tran, Duy A.,Hu, Xiaodi,Loubato, Marilia M.,Craige, Siobhan The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.2
<P>Altered energy balance and insulin resistance are important characteristics of aging. Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with muscle-specific overexpression of IL-10 (M-IL10) and in wild-type mice during hyperinsulinemic-euglycemic clamping. Despite similar fat mass and energy balance, M-IL10 mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake (similar to 60%; P < 0.05), as compared to age-matched WT mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in aging M-IL10 mice. These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings further implicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.</P>
Dagdeviren, Sezin,Jung, Dae Young,Lee, Eunjung,Friedline, Randall H.,Noh, Hye Lim,Kim, Jong Hun,Patel, Payal R.,Tsitsilianos, Nicholas,Tsitsilianos, Andrew V.,Tran, Duy A.,Tsougranis, George H.,Kearns American Society for Microbiology 2016 Molecular and cellular biology Vol.36 No.23
<P>Skeletal muscle insulin resistance is a major characteristic of obesity and type 2 diabetes. Although obesity-mediated inflammation is causally associated with insulin resistance, the underlying mechanism is unclear. Here, we examined the effects of chronic obesity in mice with muscle-specific overexpression of interleukin-10 (M-IL10). After 16 weeks of a high-fat diet (HFD), M-IL10 mice became markedly obese but showed improved insulin action compared to that of wild-type mice, which was largely due to increased glucose metabolism and reduced inflammation in skeletal muscle. Since leptin regulates inflammation, the beneficial effects of interleukin-10 (IL-10) were further examined in leptin-deficient ob/ob mice. Muscle-specific overexpression of IL-10 in ob/ob mice (MCK-IL10(ob/ob)) did not affect spontaneous obesity, but MCK-IL10(ob/ob) mice showed increased glucose turnover compared to that in ob/ob mice. Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R(-/-)) were generated to determine whether IL-10 signaling in skeletal muscle is involved in IL-10 effects on glucose metabolism. After an HFD, M-IL10R(-/-) mice developed insulin resistance with reduced glucose metabolism compared to that in wild-type mice. Overall, these results demonstrate IL-10 effects to attenuate obesity-mediated inflammation and improve insulin sensitivity in skeletal muscle, and our findings implicate a potential therapeutic role of anti-inflammatory cytokines in treating insulin resistance and type 2 diabetes.</P>
Jung, Dae Young,Ko, Hwi Jin,Lichtman, Eben I.,Lee, Eunjung,Lawton, Elizabeth,Ong, Helena,Yu, Kristine,Azuma, Yoshihiro,Friedline, Randall H.,Lee, Ki Won,Kim, Jason K. American Physiological Society 2013 AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND M Vol.304 No.9
<P>Obesity is a major cause of insulin resistance, and weight loss is shown to improve glucose homeostasis. But the underlying mechanism and the role of inflammation remain unclear. Male C57BL/6 mice were fed a high-fat diet (HFD) for 12 wk. After HFD, weight loss was induced by changing to a low-fat diet (LFD) or exercise with continuous HFD. The weight loss effects on energy balance and insulin sensitivity were determined using metabolic cages and hyperinsulinemic euglycemic clamps in awake mice. Diet and exercise intervention for 3 wk caused a modest weight loss and improved glucose homeostasis. Weight loss dramatically reduced local inflammation in skeletal muscle, liver, and heart but not in adipose tissue. Exercise-mediated weight loss increased muscle glucose metabolism without affecting Akt phosphorylation or lipid levels. LFD-mediated weight loss reduced lipid levels and improved insulin sensitivity selectively in liver. Both weight loss interventions improved cardiac glucose metabolism. These results demonstrate that a short-term weight loss with exercise or diet intervention attenuates obesity-induced local inflammation and selectively improves insulin sensitivity in skeletal muscle and liver. Our findings suggest that local factors, not adipose tissue inflammation, are involved in the beneficial effects of weight loss on glucose homeostasis.</P>