scholarly journals Body Weight Loss, Tissue Wasting and Shortened Lifespan in Late Middle-aged Mice on Imbalanced Essential/Non-essential Amino Acids Diet

2018 ◽  
Author(s):  
Giovanni Corsetti ◽  
Evasio Pasini ◽  
Claudia Romano ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
...  
Keyword(s):  
Amino Acids ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Essential Amino Acids ◽  
Skeletal Muscle Atrophy ◽  
Calorie Intake ◽  
Middle Aged ◽  
Brown Adipose ◽  
Body Wasting ◽  
The Impact

Inadequate protein intake can impair protein balance and lead to skeletal muscle atrophy, impaired body growth, and functional decline. Foods provide both non-essential (NEAAs) and essential amino acids (EAAs) that may convey different metabolic stimuli to specific organs and tissues. In this study, we sought to evaluate the impact of six diets with various EAA/NEAA blends on body composition and the risk of developing tissue wasting in late middle-aged male mice. Mice consuming NEAA-based diets, although showing increased food and calorie intake, suffered the most severe weight loss. Interestingly, even moderate NEAAs prevalence was able to induce inflammatory catabolic stimuli, generalized body wasting and systemic metabolic alterations. Complete depletion of retroperitoneal white adipose tissue and a severe loss (>75%) of brown adipose tissue were observed together with muscle wasting. Conversely, EAA-based diets induced significant decreases in weight by reducing primarily fat reserves, but improved clinical parameters. Tissue wasting was caused by altered AA quality, independent of reduced nitrogen or caloric intake. Our results indicate that an optimized balance of AA composition is necessary for preserving overall bodily energy status. These findings are particularly relevant in the context of aging and may be exploited for contrasting its negative correlates including body wasting.

scholarly journals Body Weight Loss and Tissue Wasting in Late Middle-Aged Mice on Slightly Imbalanced Essential/Non-essential Amino Acids Diet

2018 ◽  
Vol 5 ◽  
Author(s):  
Giovanni Corsetti ◽  
Evasio Pasini ◽  
Claudia Romano ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
...  
Keyword(s):  
Amino Acids ◽  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Essential Amino Acids ◽  
Middle Aged ◽  
Aged Mice

Brown adipose tissue activation in a rat model of Parkinson’s disease

2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Energy Intake ◽  
Rat Model ◽  
Sympathetic Denervation ◽  
Brown Adipose

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.

Neuroendocrine regulation of energy balance: Implications on the development and surgical treatment of obesity

2017 ◽  
Vol 23 (3) ◽  
pp. 131-146 ◽  
Author(s):  
Gisele Farias ◽  
Bárbara Dal Molin Netto ◽  
Solange Cravo Bettini ◽  
Ana Raimunda Dâmaso ◽  
Alexandre Coutinho Teixeira de Freitas
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Gastrointestinal Tract ◽  
Energy Balance ◽  
Public Health Problem ◽  
Neuroendocrine Regulation ◽  
Calorie Intake ◽  
Hormone Signaling ◽  
Sustained Weight Loss

Introduction: Obesity, a serious public health problem, occurs mainly when food consumption exceeds energy expenditure. Therefore, energy balance depends on the regulation of the hunger–satiety mechanism, which involves interconnection of the central nervous system and peripheral signals from the adipose tissue, pancreas and gastrointestinal tract, generating responses in short-term food intake and long-term energy balance. Increased body fat alters the gut- and adipose-tissue-derived hormone signaling, which promotes modifications in appetite-regulating hormones, decreasing satiety and increasing hunger senses. With the failure of conventional weight loss interventions (dietary treatment, exercise, drugs and lifestyle modifications), bariatric surgeries are well-accepted tools for the treatment of severe obesity, with long-term and sustained weight loss. Bariatric surgeries may cause weight loss due to restriction/malabsorption of nutrients from the anatomical alteration of the gastrointestinal tract that decreases energy intake, but also by other physiological factors associated with better results of the surgical procedure. Objective: This review discusses the neuroendocrine regulation of energy balance, with description of the predominant hormones and peptides involved in the control of energy balance in obesity and all currently available bariatric surgeries. Conclusions: According to the findings of our review, bariatric surgeries promote effective and sustained weight loss not only by reducing calorie intake, but also by precipitating changes in appetite control, satiation and satiety, and physiological changes in gut-, neuro- and adipose-tissue-derived hormone signaling.

scholarly journals Decreased TLR3 in Hyperplastic Adipose Tissue, Blood and Inflamed Adipocytes is Related to Metabolic Inflammation

2018 ◽  
Vol 51 (3) ◽  
pp. 1051-1068 ◽  
Author(s):  
Jèssica Latorre ◽  
José M. Moreno-Navarrete ◽  
Mónica Sabater ◽  
Maria Buxo ◽  
José I. Rodriguez-Hermosa ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Inflammation ◽  
Fat Depots ◽  
Acute Surgery ◽  
Obese Subjects ◽  
Anti Inflammatory ◽  
The Impact

Background/Aims: Obesity is characterized by the immune activation that eventually dampens insulin sensitivity and changes metabolism. This study explores the impact of different inflammatory/ anti-inflammatory paradigms on the expression of toll-like receptors (TLR) found in adipocyte cultures, adipose tissue, and blood. Methods: We evaluated by real time PCR the impact of acute surgery stress in vivo (adipose tissue) and macrophages (MCM) in vitro (adipocytes). Weight loss was chosen as an anti-inflammatory model, so TLR were analyzed in fat samples collected before and after bariatric surgery-induced weight loss. Associations with inflammatory and metabolic parameters were analyzed in non-obese and obese subjects, in parallel with gene expression measures taken in blood and isolated adipocytes/ stromal-vascular cells (SVC). Treatments with an agonist of TLR3 were conducted in human adipocyte cultures under normal conditions and upon conditions that simulated the chronic low-grade inflammatory state of obesity. Results: Surgery stress raised TLR1 and TLR8 in subcutaneous (SAT), and TLR2 in SAT and visceral (VAT) adipose tissue, while decreasing VAT TLR3 and TLR4. MCM led to increased TLR2 and diminished TLR3, TLR4, and TLR5 expressions in human adipocytes. The anti-inflammatory impact of weight loss was concomitant with decreased TLR1, TLR3, and TLR8 in SAT. Cross-sectional associations confirmed increased V/ SAT TLR1 and TLR8, and decreased TLR3 in obese patients, as compared with non-obese subjects. As expected, TLR were predominant in SVC and adipocyte precursor cells, even though expression of all of them but TLR8 (very low levels) was also found in ex vivo isolated and in vitro differentiated adipocytes. Among SVC, CD14+ macrophages showed increased TLR1, TLR2, and TLR7, but decreased TLR3 mRNA. The opposite patterns shown for TLR2 and TLR3 in V/ SAT, SVC, and inflamed adipocytes were observed in blood as well, being TLR3 more likely linked to lymphocyte instead of neutrophil counts. On the other hand, decreased TLR3 in adipocytes challenged with MCM dampened lipogenesis and the inflammatory response to Poly(I:C). Conclusion: Functional variations in the expression of TLR found in blood and hypertrophied fat depots, namely decreased TLR3 in lymphocytes and inflamed adipocytes, are linked to metabolic inflammation.

scholarly journals Importance of brown adipose tissue to the thermal effect and weight loss induced by central administration of C75

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Priscila Cassolla ◽  
Maria Antonieta R. Garófalo ◽  
Juliana B. Guimarães ◽  
Frederico S. M. Machado ◽  
Coimbra C. Cândido ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Thermal Effect ◽  
Central Administration ◽  
Brown Adipose

scholarly journals Impaired Thermogenesis and a Molecular Signature for Brown Adipose Tissue inId2Null Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Peng Zhou ◽  
Maricela Robles-Murguia ◽  
Deepa Mathew ◽  
Giles E. Duffield
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Energy Homeostasis ◽  
Core Body Temperature ◽  
Specific Pattern ◽  
Molecular Signature ◽  
Brown Adipose ◽  
Core Body ◽  
The Impact

Inhibitor of DNA binding 2 (ID2) is a helix-loop-helix transcriptional repressor rhythmically expressed in many adult tissues. Our previous studies have demonstrated thatId2null mice have sex-specific elevated glucose uptake in brown adipose tissue (BAT). Here we further explored the role ofId2in the regulation of core body temperature over the circadian cycle and the impact ofId2deficiency on genes involved in insulin signaling and adipogenesis in BAT. We discovered a reduced core body temperature inId2−/− mice. Moreover, inId2−/− BAT, 30 genes includingIrs1,PPARs, andPGC-1s were identified as differentially expressed in a sex-specific pattern. These data provide valuable insights into the impact ofId2deficiency on energy homeostasis of mice in a sex-specific manner.

Abstract 12656: Phosphodiesterase 4 (PDE4) Inhibition Induces Weight Loss and Improves Insulin Resistance via cAMP-EPAC-AMPK Mediated Reprogramming of Macrophages

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Chaoneng Wu ◽  
Andrei Maiseyeu ◽  
Jeffrey A Deiuliis ◽  
Jixin Zhong ◽  
Xiaoquan Rao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Catecholamine Release ◽  
Innate Immune ◽  
Chow Diet ◽  
Intracellular Camp ◽  
Mouse Bone Marrow ◽  
Phosphodiesterase 4 ◽  
Brown Adipose

Objective: Recent evidence suggests an important role for cAMP-dependent pathways in modulation of innate immune function. Phosphodiesterase 4 (PDE4) is widely expressed in innate immune cells such as macrophages/dendritic cells with potent anti-inflammatory effects on pharmacologic inhibition of the enzyme. We investigated the importance of PDE4 in diet-induced obesity (DIO) and hypothesized that PDE4 inhibition will improve insulin sensitivity and reduce inflammation. Methods and Results: PDE4 was upregulated in both visceral and subcutaneous (SubQ) white adipose tissue (WAT) in DIO mice (12 weeks of high-fat diet, HFD, 60% fat) compared to normal-chow diet (NCD) mice (↑4∼10-folds, p<0.01). The degree of expression was correlated with macrophage infiltration in stromal vascular fraction from WAT (CD11b + F4/80 + cells, r=0.56, p<0.05). Treatment with Roflumilast (3mg/kg/day), a high affinity inhibitor of PDE4 (IC 50 0.39 nM) versus vehicle control (n=6∼10 in each group) for 21 days concomitant with HFD, resulted in rapid and substantial weight loss (↓45.8% fat content), enhanced thermogenesis [(∼20% higher oxygen consumption and heat production, 0.7∼1.1°C higher core body temperature in a cold environment (4°C)], brown adipose reprogramming, improvement in insulin resistance (HOMA-IR ↓ from 0.69±0.04 to 0.44±0.01, p<0.01) and hepatic steatosis. These changes were paralleled by increased alternative macrophage activation (Altf), reduced inflammation in WAT [↑CD206 and CD301 by flow cytometry with ↓ TNF/IL-6 gene expression] and activation of thermogenic genes in brown adipose tissue. In-vitro treatment of mouse bone marrow-derived macrophages (BMDM) promoted Altf and increased expression of tyrosine hydroxylase (↑2.5 folds) and catecholamines secretion. Additional experiments with agents that augment/reduce intracellular cAMP/EPAC/AMPK revealed an essential role for this cascade in Altf activation and catecholamine release. Conclusions: PDE4 antagonism improves obese diabetic symptoms through convergent pathways involving Altf activation and enhancing thermogenesis via cAMP dependent modulation of macrophage catecholamine release.

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