Leucine supplementation improves adiponectin and total cholesterol concentrations despite the lack of changes in adiposity or glucose homeostasis in rats previously exposed to a high-fat diet

Leal, Francisco; Fonseca‐Alaniz, Miriam Helena; Teodoro, Gabriela Fullin Resende; Capitani, Mariana Dutilh de; Vianna, Daiana; Pantaleão, Lucas Carminatti; Matos-Neto, Emídio Marques de; Rogero, Marcelo Macedo; Donato, José; Tirapegui, Júlio

doi:10.1186/1743-7075-8-62

Cited by 66 publications

(54 citation statements)

References 45 publications

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“…In diet-induced obesity, leptin levels are high, reflecting increased fat depots (Myers et al, 2010;Torres-Leal et al, 2011). Studies in healthy humans have demonstrated that moderate weight gain increases the expression of adipokines and alters the expression of caveolin 1 in WAT.…”

Section: Leptinmentioning

confidence: 99%

Obesity, inflammation, and insulin resistance

Martins

Oliveira

Cruz

et al. 2014

Braz. J. Pharm. Sci.

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White adipose tissue (WAT) is considered an endocrine organ. When present in excess, WAT can influence metabolism via biologically active molecules. Following unregulated production of such molecules, adipose tissue dysfunction results, contributing to complications associated with obesity. Previous studies have implicated pro-and anti-inflammatory substances in the regulation of inflammatory response and in the development of insulin resistance. In obese individuals, pro-inflammatory molecules produced by adipose tissue contribute to the development of insulin resistance and increased risk of cardiovascular disease. On the other hand, the molecules with anti-inflammatory action, that have been associated with the improvement of insulin sensitivity, have your decreased production. Imbalance of these substances contributes significantly to metabolic disorders found in obese individuals. The current review aims to provide updated information regarding the activity of biomolecules produced by WAT.Uniterms: Obesity. Inflammation. Adipose tissue. Adipokines. Insulin resistance.O tecido adiposo branco (WAT) é considerado um órgão endócrino, que, em excesso, é capaz de controlar o metabolismo, pela ação de moléculas biologicamente ativas. A produção desregulada destas substâncias pela disfunção do tecido adiposo pode contribuir para as complicações presentes na obesidade. As pesquisas atuais têm esclarecido fatores e mecanismos envolvidos na atuação de substâncias pró e anti-inflamatórias na modulação da inflamação e da resistência à insulina. Em indivíduos obesos, as moléculas pró-inflamatórias produzidas pelo tecido adiposo têm sido implicadas como fator contribuinte para o desenvolvimento da resistência à insulina e aumento do risco de doença cardiovascular. Por outro lado, as moléculas com ação anti-inflamatória, que atuam na melhora da sensibilidade à insulina, têm sua produção reduzida. O desequilíbrio entre essas substâncias contribui de forma significativa para as desordens metabólicas presente em indivíduos obesos. Assim, esta revisão visa a trazer informações atualizadas sobre a atuação de moléculas secretadas pelo tecido adiposo. Unitermos:Obesidade. Inflamação. Tecido adiposo. Adipocinas. Resistência à insulina.

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Section: Leptinmentioning

confidence: 99%

Obesity, inflammation, and insulin resistance

Martins

Oliveira

Cruz

et al. 2014

Braz. J. Pharm. Sci.

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“…These findings are supported by previous reports showing beneficial effects of branched amino acids and the primary ingredients of ketoacid supplements on systemic inflammation. For example, leucine administration has been reported to decrease serum tumor necrosis factor-alpha (TNF-α) and increase serum adiponectin levels in animal models (15). Similarly, in overweight or obese subjects, leucine and pyridoxine combination administered for 4 weeks improved insulin resistance, accompanied by reduced inflammatory markers (TNF-α and CRP) and increased adiponectin levels (16).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the keto-analogs of essential amino acids could also have direct effects on insulin sensitivity (12)(13)(14). Further, components of ketoacid supplementation could improve other co-existing metabolic abnormalities such as inflammation and oxidative stress (15)(16)(17) and could indirectly prevent worsening of insulin resistance. There are currently no studies examining beneficial metabolic effects of ketoacid supplementation with a regular protein diet in PD patients.…”

mentioning

confidence: 99%

Ketoacid Supplementation Partially Improves Metabolic Parameters in Patients on Peritoneal Dialysis

Dong

et al. 2015

Perit Dial Int

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♦ Background: A low protein diet supplemented with ketoacids has been shown to improve the metabolic profile, including insulin resistance, in patients with chronic kidney disease (CKD), but whether ketoacids alone exert similar effects is unknown. In this prospective randomized controlled trial, we aimed to evaluate the effects of ketoacid supplementation on insulin resistance, systemic inflammation, oxidative stress and endothelial dysfunction among 100 CKD patients undergoing peritoneal dialysis (PD). ♦ Methods: Patients from one Chinese PD center were randomly assigned to take ketoacids (12 tablets per day) (n = 50) versus a control group (n = 50) for 6 months in an open-label parallelarm design. Daily protein intake of 0.8 -1.2 g/kg/d and daily energy intake of 25 -35 kcal/kg/d was prescribed to both groups. Insulin resistance was evaluated using homeostatic model assessment (HOMA-IR) index as the primary outcome. We assessed systemic inflammation using high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6), oxidative stress using plasma oxidized low density lipoprotein (oxLDL), adipokines using leptin and adiponectin and endothelial dysfunction using serum soluble intercellular adhesion molecule-1 (sICAM) and soluble vascular adhesion molecule-1 (sVCAM) as secondary outcomes. ♦ Results: There were no significant differences in baseline characteristics between the 2 groups except a slightly higher age in patients assigned to the intervention. A total of 89% of participants completed the 6-month intervention. There was no significant difference in the change of HOMA-IR values from baseline between groups after adjusting for baseline age, gender, body mass index and HOMA-IR. For secondary outcomes, hs-CRP varied significantly between groups (p = 0.02), increasing over time for the control group while remaining stable for the ketoacid group. Similarly, the leptin/adiponectin ratio (LAR) differed between groups (p < 0.001), remaining stable in the ketoacid group but increasing in the control group. ♦ Conclusion: Ketoacid therapy administered for 6 months had no effect on HOMA-IR but resulted in improvements in hs-CRP and LAR, suggesting metabolic benefit. Future studies are needed to confirm these results and any potential benefit in vascular health of PD patients.

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“…Leucine administration (Figure 3) has been shown to stimulate insulin release [191] [192] increase adiponectin levels and reduce cholesterol levels in rats and glucose levels in obese mice [193]- [195]. Interest in leucine administration in man has increased with the effects of leucine on food intake and appetite control that involves the hypothalamus [196] [197].…”

Section: Nutritional Interventions Reverse Nafld With the Prevention mentioning

confidence: 99%

Induction of NAFLD with Increased Risk of Obesity and Chronic Diseases in Developed Countries

Martins¹

2014

OJEMD

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The susceptibility of individuals to obesity has been reported in many developed countries with predisposition of humans to obesity associated with high calorie diets and unhealthy lifestyles. Obesity may closely be involved in cell suicide in various organ diseases with the importance of accelerated aging that requires early intervention with drug therapy to prevent diseases such as non alcoholic fatty liver disease (NAFLD) that has increased in children and reached to approx. 40% of the global population. Obesity is induced by various diets and lifestyle factors such as stress, anxiety and depression which are important to consider with the global increase in obesity and are possibly linked to the rise in individuals with brain disorders that involve neurodegeneration. Xenobiotics such as the endocrine disruptor chemicals that have increased in the environment in various developed countries lead to various chronic endocrine diseases as populations divert towards unhealthy diets and lifestyles with induction of NAFLD and obesity. The amount and nature of food intake that improves and increases liver lipid and xenobiotic metabolism in obese individuals have become important to decrease the risk for increased adiposity in man. High fibre or protein diets that contain leucine may improve liver glucose, lipid and xenobiotic metabolism and require further investigation with xenobiotics such as endocrine disruptors involved in appetite dysregulation and metabolic disorders in developed countries. The use of anti-obese drugs that reduce food intake and improve hypercholesterolemia and cardiovascular disease has been assessed in obesity with drug therapy closely involved either in the prevention or induction of NAFLD and obesity in man.

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Leucine supplementation improves adiponectin and total cholesterol concentrations despite the lack of changes in adiposity or glucose homeostasis in rats previously exposed to a high-fat diet

Cited by 66 publications

References 45 publications

Obesity, inflammation, and insulin resistance

Obesity, inflammation, and insulin resistance

Ketoacid Supplementation Partially Improves Metabolic Parameters in Patients on Peritoneal Dialysis

Induction of NAFLD with Increased Risk of Obesity and Chronic Diseases in Developed Countries

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