scholarly journals The Effects of High-Protein Diet and Resistance Training on Glucose Control and Inflammatory Profile of Visceral Adipose Tissue in Rats

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1969
Author(s):  
Claudia Stela Medeiros ◽  
Ivo Vieira de Sousa Neto ◽  
Keemilyn Karla Santos Silva ◽  
Ana Paula Castro Cantuária ◽  
Taia Maria Berto Rezende ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Resistance Training ◽  
Glucose Intolerance ◽  
Glucose Control ◽  
Muscle Protein ◽  
Blood Glucose Control ◽  
High Protein ◽  
Epididymal Adipose Tissue ◽  
Adipocyte Size ◽  
The Impact

High-protein diets (HPDs) are widely accepted as a way to stimulate muscle protein synthesis when combined with resistance training (RT). However, the effects of HPDs on adipose tissue plasticity and local inflammation are yet to be determined. This study investigated the impact of HPDs on glucose control, adipocyte size, and epididymal adipose inflammatory biomarkers in resistance-trained rats. Eighteen Wistar rats were randomly assigned to four groups: normal-protein (NPD; 17% protein total dietary intake) and HPD (26.1% protein) without RT and NPD and HPD with RT. Trained groups received RT for 12 weeks with weights secured to their tails. Glucose and insulin tolerance tests, adipocyte size, and an array of cytokines were determined. While HPD without RT induced glucose intolerance, enlarged adipocytes, and increased TNF-α, MCP-1, and IL1-β levels in epididymal adipose tissue (p < 0.05), RT diminished these deleterious effects, with the HPD + RT group displaying improved blood glucose control without inflammatory cytokine increases in epididymal adipose tissue (p < 0.05). Furthermore, RT increased glutathione expression independent of diet (p < 0.05). RT may offer protection against adipocyte hypertrophy, pro-inflammatory states, and glucose intolerance during HPDs. The results highlight the potential protective effects of RT to mitigate the maladaptive effects of HPDs.

scholarly journals Developmental androgen excess programs sympathetic tone and adipose tissue dysfunction and predisposes to a cardiometabolic syndrome in female mice

2013 ◽  
Vol 304 (12) ◽  
pp. E1321-E1330 ◽  
Author(s):  
Kazunari Nohara ◽  
Rizwana S. Waraich ◽  
Suhuan Liu ◽  
Mathieu Ferron ◽  
Aurélie Waget ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Intolerance ◽  
Adult Female ◽  
Sympathetic Tone ◽  
Visceral Adiposity ◽  
Androgen Excess ◽  
Altered Expression ◽  
Female Mice ◽  
The Impact

Among women, the polycystic ovarian syndrome (PCOS) is considered a form of metabolic syndrome with reproductive abnormalities. Women with PCOS show increased sympathetic tone, visceral adiposity with enlarged adipocytes, hypoadiponectinemia, insulin resistance, glucose intolerance, increased inactive osteocalcin, and hypertension. Excess fetal exposure to androgens has been hypothesized to play a role in the pathogenesis of PCOS. Previously, we showed that neonatal exposure to the androgen testosterone (NT) programs leptin resistance in adult female mice. Here, we studied the impact of NT on lean and adipose tissues, sympathetic tone in cardiometabolic tissues, and the development of metabolic dysfunction in mice. Neonatally androgenized adult female mice (NTF) displayed masculinization of lean tissues with increased cardiac and skeletal muscle as well as kidney masses. NTF mice showed increased and dysfunctional white adipose tissue with increased sympathetic tone in both visceral and subcutaneous fat as well as increased number of enlarged and insulin-resistant adipocytes that displayed altered expression of developmental genes and hypoadiponectinemia. NTF exhibited dysfunctional brown adipose tissue with increased mass and decreased energy expenditure. They also displayed decreased undercarboxylated and active osteocalcin and were predisposed to obesity during chronic androgen excess. NTF showed increased renal sympathetic tone associated with increased blood pressure, and they developed glucose intolerance and insulin resistance. Thus, developmental exposure to testosterone in female mice programs features of cardiometabolic dysfunction, as can be observed in women with PCOS, including increased sympathetic tone, visceral adiposity, insulin resistance, prediabetes, and hypertension.

scholarly journals Saline versus 5% dextrose in water as a drug diluent for critically ill patients: a retrospective cohort study

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Yukari Aoyagi ◽  
Takuo Yoshida ◽  
Shigehiko Uchino ◽  
Masanori Takinami ◽  
Shoichi Uezono
Keyword(s):  
Blood Glucose ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Glucose Control ◽  
Blood Glucose Control ◽  
Kidney Injury ◽  
Saline Group ◽  
Significant Difference ◽  
The Impact ◽  
Electrolyte Abnormalities

Abstract Background The choice of intravenous infusion products for critically ill patients has been studied extensively because it can affect prognosis. However, there has been little research on drug diluents in this context. The purpose of this study is to evaluate the impact of diluent choice (saline or 5% dextrose in water [D5W]) on electrolyte abnormalities, blood glucose control, incidence of acute kidney injury (AKI), and mortality. Methods This before-after, two-group comparative, retrospective study enrolled adult patients who stayed for more than 48 h in a general intensive care unit from July 2015 to December 2018. We changed the default diluent for intermittent drug sets in our electronic ordering system from D5W to saline at the end of 2016. Results We included 844 patients: 365 in the D5W period and 479 in the saline period. Drug diluents accounted for 21.4% of the total infusion volume. The incidences of hypernatremia and hyperchloremia were significantly greater in the saline group compared to the D5W group (hypernatremia 27.3% vs. 14.6%, p < 0.001; hyperchloremia 36.9 % vs. 20.4%, p < 0.001). Multivariate analyses confirmed the similar effects (hypernatremia adjusted odds ratio (OR), 2.43; 95% confidence interval (CI), 1.54–3.82; hyperchloremia adjusted OR, 2.09; 95% CI, 1.31–3.34). There was no significant difference in the incidences of hyperglycemia, AKI, and mortality between the two groups. Conclusions Changing the diluent default from D5W to saline had no effect on blood glucose control and increased the incidences of hypernatremia and hyperchloremia.

Mechanism of enhanced lipolysis in adipose tissue of exercise-trained rats

1980 ◽  
Vol 239 (6) ◽  
pp. E422-E429 ◽  
Author(s):  
L. Bukowiecki ◽  
J. Lupien ◽  
N. Follea ◽  
A. Paradis ◽  
D. Richard ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Food Restriction ◽  
Female Rats ◽  
Epididymal Adipose Tissue ◽  
Adipocyte Size ◽  
Fat Depots ◽  
Male And Female Rats ◽  
Receptor Sites ◽  
Stimulus Recognition

The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.

Resistance training minimizes catabolic effects induced by sleep deprivation in rats

2015 ◽  
Vol 40 (11) ◽  
pp. 1143-1150 ◽  
Author(s):  
Marcos Mônico-Neto ◽  
Hanna Karen Moreira Antunes ◽  
Kil Sun Lee ◽  
Stuart M. Phillips ◽  
Sara Quaglia de Campos Giampá ◽  
...  
Keyword(s):  
Weight Loss ◽  
Resistance Training ◽  
Sleep Deprivation ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Synthetic Activity ◽  
Control Group ◽  
The Impact

Sleep deprivation (SD) can induce muscle atrophy. We aimed to investigate the changes underpinning SD-induced muscle atrophy and the impact of this condition on rats that were previously submitted to resistance training (RT). Adult male Wistar EPM-1 rats were randomly allocated into 1 of 5 groups: control, sham, SD (for 96 h), RT, and RT+SD. The major outcomes of this study were muscle fiber cross-sectional area (CSA), anabolic and catabolic hormone profiles, and the abundance of select proteins involved in muscle protein synthesis and degradation pathways. SD resulted in muscle atrophy; however, when SD was combined with RT, the reduction in muscle fiber CSA was attenuated. The levels of IGF-1 and testosterone were reduced in SD animals, and the RT+SD group had higher levels of these hormones than the SD group. Corticosterone was increased in the SD group compared with the control group, and this increase was minimized in the RT+SD group. The increases in corticosterone concentrations paralleled changes in the abundance of ubiquitinated proteins and the autophagic proteins LC3 and p62/SQSTM1, suggesting that corticosterone may trigger these changes. SD induced weight loss, but this loss was minimized in the RT+SD group. We conclude that SD induced muscle atrophy, probably because of the increased corticosterone and catabolic signal. High-intensity RT performed before SD was beneficial in containing muscle loss induced by SD. It also minimized the catabolic signal and increased synthetic activity, thereby minimizing the body’s weight loss.

Modulation of adipocyte size and fat pad weight via resveratrol releasing scaffolds implanted into the epididymal adipose tissue

2020 ◽  
Author(s):  
Kendall P. Murphy ◽  
Michael A. Hendley ◽  
Alexandra T. Patterson ◽  
Hayley E. Hall ◽  
Griffin J. Carter ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Adipocyte Size ◽  
Fat Pad

The impact of blood glucose control on fetal growth in gestational diabetes

1997 ◽  
Vol 176 (1) ◽  
pp. S182
Author(s):  
MY Divon ◽  
K Feisullin ◽  
A Bernstein ◽  
S Scarpelli ◽  
D Sherer ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gestational Diabetes ◽  
Fetal Growth ◽  
Glucose Control ◽  
Blood Glucose Control ◽  
The Impact

scholarly journals Pinch Loss Ameliorates Obesity, Glucose Intolerance and Fatty Liver by Modulating Adipocyte Apoptosis in Mice

2021 ◽  
Author(s):  
Huanqing Gao ◽  
Yiming Zhong ◽  
Zhen Ding ◽  
Sixiong Lin ◽  
Xiaoting Hou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Liver ◽  
Glucose Intolerance ◽  
Metabolic Diseases ◽  
Caspase 8 ◽  
Chow Diet ◽  
Adipocyte Size ◽  
Genetic Ablation ◽  
Brown Adipose

The mammalian focal adhesion proteins Pinch1/2 activate integrins and promote cell-ECM adhesion and migration; however, their roles in adipose tissue and metabolism are unclear. Here we find that high fat diet (HFD) feeding dramatically increases expression of Pinch1/2 proteins in white adipose tissues (WAT) in mice. Furthermore, expression of Pinch1 is largely up-regulated in WAT in the Leptin-deficient ob/ob type 2 diabetic mice and obese humans. While mice with the loss of Pinch1 in adipocytes or global Pinch2 do not display any notable phenotypes, deleting Pinch1 in adipocytes and Pinch2 globally significantly decreases body weight and WAT, but not brown adipose tissue (BAT), mass in HFD-, but not normal chow diet (NCD)-, fed mice. Pinch loss ameliorates HFD-induced glucose intolerance and fatty liver. After HFD challenge, Pinch loss slightly, but significantly, accelerates energy expenditure. While Pinch loss decreases adipocyte size and alters adipocyte size distribution, it greatly accelerates cell apoptosis primarily in epididymal WAT and to a less extent subcutaneous WAT. In vitro studies demonstrate that Pinch loss accelerates adipocyte apoptosis by activating the Bim/Caspase-8 pathway. In vivo, genetic ablation of Caspase-8 expression in adipocytes essentially abolishes the ameliorating effects of Pinch deficiency on obesity, glucose intolerance and fatty liver in mice. Thus, we demonstrate a previously unknown function of Pinch in control of adipose mass, glucose and fat metabolism via modulation of adipocyte apoptosis. We may define a novel target for the prevention and treatment of metabolic diseases, such as obesity and diabetics.

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