scholarly journals Subcutaneous adipose tissue accumulation protects systemic glucose tolerance and muscle metabolism

Adipocyte ◽  
2018 ◽  
Vol 7 (4) ◽  
pp. 261-272 ◽  
Author(s):  
A.D. Booth ◽  
A.M. Magnuson ◽  
J. Fouts ◽  
Y. Wei ◽  
D. Wang ◽  
...  
1990 ◽  
Vol 70 (1) ◽  
pp. 199-206 ◽  
Author(s):  
O. ADEOLA ◽  
B. W. McBRIDE ◽  
R. O. BALL ◽  
L. G. YOUNG

Subcutaneous adipose tissue and intercostal and sartorius muscles from five barrows and five gilts at 20 kg liveweight were used to study lipogenesis, lipolysis, Na+, K+-ATPase-dependent respiration and protein synthesis. Lipogenesis rate measured by 14C-acetate incorporation into lipid was similar between barrows and gilts; and 100 μg insulin per mL enhanced (P < 0.1) subcutaneous adipose tissue lipogenesis by 74%. Lipolysis rate quantitated by glycerol release was similar between barrows and gilts (3546 and 4160 nmol g−1 2 h−1). Adenosine deaminase and norepinephrine together enhanced adipose tissue lipolytic response by 102%. Fractional and absolute rates of protein synthesis were similar between barrows and gilts (3.24 and 3.69% d−1; 6.01 and 6.06 mg g−1 d−1); and between intercostal and sartorius muscles. Barrows had lower Na+, K+-ATPase-dependent respiration than gilts and the maintenance of Na+ and K+ transmembrane ionic gradient in the muscle preparations accounted for 23–26% of total respiration. Key words: Pigs, adipose tissue, skeletal muscle, metabolism


2005 ◽  
Vol 288 (5) ◽  
pp. E930-E934 ◽  
Author(s):  
Neda Rasouli ◽  
Ulrika Raue ◽  
Leslie M. Miles ◽  
Tong Lu ◽  
Gina B. Di Gregorio ◽  
...  

Patients with insulin resistance often manifest increased intramyocellular lipid (IMCL) along with increased visceral adipose tissue. This study was designed to determine whether the insulin sensitizer drugs pioglitazone and metformin would improve glucose intolerance and insulin sensitivity by decreasing IMCL. In this study, 23 generally healthy subjects with impaired glucose tolerance were randomized to receive either pioglitazone 45 mg/day or metformin 2,000 mg/day for 10 wk. Before and after treatment, we measured insulin sensitivity and abdominal subcutaneous and visceral adipose tissue with CT scanning. In addition, muscle biopsies were performed for measurement of IMCL and muscle oxidative enzymes. After treatment with pioglitazone, 2-h glucose fell from 9.6 mmol/l (172 mg/dl) to 6.1 mmol/l (119 mg/dl), whereas there was no change in 2-h glucose with metformin. With pioglitazone treatment, there was a 65% increase in insulin sensitivity along with a 34% decrease in IMCL (both P ≤ 0.002). This decrease in IMCL was not due to increased muscle lipid oxidation, as there were no changes in muscle lipid oxidative enzymes. However, pioglitazone resulted in a 2.6-kg weight gain along with a significant decrease in the visceral-to-subcutaneous adipose tissue ratio. In contrast, metformin treatment resulted in no change in insulin sensitivity, IMCL, oxidative enzymes, or adipose tissue volumes. Pioglitazone improved glucose tolerance and insulin sensitivity by reducing IMCL. This reduction in IMCL was not due to an increase in muscle lipid oxidation but to a diversion of lipid from ectopic sites into subcutaneous adipose tissue.


2017 ◽  
Vol 233 (3) ◽  
pp. 269-279 ◽  
Author(s):  
Greg M Kowalski ◽  
Michael J Kraakman ◽  
Shaun A Mason ◽  
Andrew J Murphy ◽  
Clinton R Bruce

The high-fat, high-sucrose diet (HFSD)–fed C57Bl/6 mouse is a widely used model of prediabetes. However, studies typically implement a relatively short dietary intervention lasting between 4 and 16 weeks; as a result, little is known about how a long-term HFSD influences the metabolic profile of these mice. Therefore, the aim of this investigation was to examine the effects of consuming a HFSD for 42 weeks on the development of hyperinsulinaemia and glucose intolerance in male C57Bl/6 mice. Two cohorts of HFSD mice were studied at independent institutes and they underwent an oral glucose tolerance test (OGTT) with measures of plasma insulin and free fatty acids (FFA). Age-matched chow-fed control mice were also studied. The HFSD-fed mice were hyperinsulinaemic and grossly obese, being over 25 g heavier than chow-fed mice, which was due to a marked expansion of subcutaneous adipose tissue. This was associated with a 3-fold increase in liver lipid content. Glucose tolerance, however, was either the same or better than control mice due to the preservation of glucose disposal as revealed by a dynamic stable isotope-labelled OGTT. In addition, plasma FFAs were suppressed to lower levels in HFSD mice during the OGTT. In conclusion, we have made the paradoxical observation that long-term HFSD feeding results in the resolution of glucose intolerance in the C57Bl/6 mouse. Mechanistically, we propose that the gross expansion of subcutaneous adipose tissue increases the glucose disposal capacity of the HFSD-fed mouse, which overcomes the prevailing insulin resistance to improve glucose tolerance.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1262-1262
Author(s):  
Yujiao Zu ◽  
Mandana Pahlavani ◽  
Latha Ramalingam ◽  
Shane Scoggin ◽  
Naima Moustaid-Moussa

Abstract Objectives Activation and recruitment of thermogenic cells in white adipose tissue (WAT browning), in response to cold exposure, can combat obesity and associated metabolic disorders. We have previously reported that the beneficial effects of eicosapentaenoic acid (EPA), a long-chain omega 3 polyunsaturated fatty acids, in obesity and insulin resistance are independent of UCP1. In this study, we investigate the protective effects of EPA and the role of UCP1 in the browning of subcutaneous adipose tissue (SAT) at ambient and thermoneutral environments using UCP1 knockout (KO) mice. We hypothesized that EPA promotes SAT browning to prevent diet-induced obesity at both temperatures, independently of UCP1. Methods Male and UCP1 KO and wild type (WT) B6 littermates were housed at room temperature (22°C) or thermoneutrality (28–30°C) and fed a high fat (HF) diet (45% kcal fat) supplemented with or without EPA (36g/kg) for 14 weeks. Body weight and glucose tolerance test (GTT) were measured, and browning-related markers were assessed in SAT. Data were statistically analyzed via three-way ANOVA using GraphPad to determine the individual and interactive effects of temperature, genotype, and diet. Results Compared to the WT, the body weight (BW) of KO mice increased at thermoneutrality (P &lt; 0.01) but decreased at ambient temperature (P &lt; 0.0001). Additionally, EPA attenuated weight and fat mass gain at thermoneutrality and improved glucose tolerance at both temperatures in both genotypes. mRNA levels for brown fat markers (Dio2 and Cidea), lipid metabolism (Elovl3, PGC1α, FASN, Cpt1b, and Gpd1), and batokines (Bmp8b and FGF21) were significantly up-regulated in KO mice, compared to WT, at ambient temperature (P &lt; 0.01). Moreover, compared to HF-fed mice, EPA increased above markers in the KO mice at ambient temperature. Compared to HF, EPA-fed mice had significantly higher serum adiponectin levels (P &lt; 0.01) in both genotypes and temperatures. Conclusions UCP1 KO male mice were protected from diet-induced obesity and glucose intolerance and had increased SAT browning at ambient temperature. These results indicate that alternative thermoregulatory pathways mediate protective metabolic effects of EPA, in the absence of UCP1. These findings may be translated to human subjects with obesity, who exhibit low amounts of brown fat and UCP1. Funding Sources NIH R15AT008879-01A1.


2014 ◽  
Author(s):  
Ana Valeria B Castro ◽  
Vania S Nunes ◽  
Viorica Ionut ◽  
Richard N Bergman ◽  
Regina El Dib

BACKGROUND: Several lines of evidence show that abdominal fat is strongly associated with insulin resistance and dysglycemia (impaired glucose tolerance - IGT or type 2 diabetes mellitus - T2DM). However, which component of abdominal fat, subcutaneous or intra-abdominal, has a major impact on the development of insulin resistance and dysglycemia is still a matter of debate. The aim of this review is to summarize the best available evidence on the contribution of subcutaneous and/or intra-abdominal adipose tissues to the incidence of impaired glucose tolerance and/or type 2 diabetes mellitus, in adults as well as to determine which type of abdominal fat is a better predictor of these metabolic disorders. METHODS: A search of published articles on PUBMED (1966 to June 2013), EMBASE (1980 to June 2013), LILACS (1982 to June 2013) and Central Cochrane databases was conducted to identify studies evaluating the relationship between intra-abdominal and/or subcutaneous adipose tissue and the incident IGT or T2DM). Cohort studies examining the association between intra-abdominal and/or subcutaneous adipose tissue values and the prospective development of impaired glucose tolerance or type 2 diabetes mellitus (estimated risk) were included in this review. Data extraction and risk of bias assessments were performed in duplicate by 2 reviewers. Random-effects meta-analyses were performed to pool OR estimates from individual studies to assess the association between intra-abdominal and/or subcutaneous adipose tissue values at baseline and the risk of development of impaired glucose tolerance or type 2 diabetes mellitus. Statistical heterogeneity was assessed using the I2 statistics. The risk of bias was assessed by examining the sample selected, recruitment method, completeness of follow up and blinding according to the guidelines for assessing quality in prognostic studies proposed by Hayden (29) and the MOOSE (30) statement, and adapted by us. RESULTS: Five relevant studies were suitable for this review. The analysis showed that both VAT and abdominal SAT measurements at baseline were strong predictors of incident impaired glucose tolerance or type 2 diabetes mellitus, in minimally adjusted models. However, when other confounding variables besides age, sex and ethnicity were taken into account, VAT, but not SAT, measurements pose a high risk of the incident IGT or T2DM in a wide range of age and ethnic backgrounds (Japanese-, Hispanic-, African-Americans and Canadians). CONCLUSIONS: In conclusion, the present results provide some evidence that VAT imposes more risk to the development of IGT and T2DM than abdominal SAT. However, more studies are necessary to confirm these results and to address the issue of changes in VAT and abdominal SAT and their predictive value regarding IGT and type 2 diabetes developments.


Obesity Facts ◽  
2008 ◽  
Vol 1 (6) ◽  
pp. 310-318 ◽  
Author(s):  
Étienne Pigeon ◽  
Érick Couillard ◽  
Angelo Tremblay ◽  
Claude Bouchard ◽  
S.John Weisnagel ◽  
...  

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