Plasma Cholesterol- and Body Fat-Lowering Effects of Chicken Protein Hydrolysate and Oil in High-Fat Fed Male Wistar Rats.

Rest raw materials provide a new source of bioactive dietary ingredients, and this study aimed to determine the health effects of diets with chicken protein hydrolysate (CPH) and chicken oil (CO) generated from deboned chicken meat. Male Wistar rats (n = 56) were divided into seven groups in three predefined sub-experiments to study the effects of protein source (casein, chicken fillet, pork fillet, and CPH), the dose-effect of CPH (50% and 100% CPH), and the effects of combining CPH and CO. Rats were fed high-fat diets for 12 weeks, and casein and chicken fillet were used as controls in all sub-experiments. While casein, chicken-, or pork fillet diets resulted in similar weight gain and plasma lipid levels, the CPH diet reduced plasma total cholesterol. This effect was dose dependent and accompanied with the reduced hepatic activities of acetyl-CoA carboxylase and fatty acid synthase. Further, rats fed combined CPH and CO showed lower weight gain, and higher hepatic mitochondrial fatty acid oxidation, plasma L-carnitine, short-chain acylcarnitines, TMAO, and acetylcarnitine/palmitoylcarnitine. Thus, in male Wistar rats, CPH and CO lowered plasma cholesterol and increased hepatic fatty acid oxidation compared to whole protein diets, pointing to potential health-beneficial bioactive properties of these processed chicken rest raw materials.

Plasma 3-hydroxyisobutyrate (3-HIB) and methylmalonic acid (MMA) are markers of hepatic mitochondrial fatty acid oxidation in male Wistar rats.

OBJECTIVE: Discovery of specific markers that reflect altered hepatic fatty acid oxidation could help to detect an individual's risk of fatty liver, type 2 diabetes and cardiovascular disease at an early stage. Lipid and protein metabolism are intimately linked, but our understanding of this crosstalk remains limited. METHODS: In male Wistar rats, we used synthetic fatty acid analogues (3-thia fatty acids) as a tool to induce hepatic fatty acid oxidation and mitochondrial biogenesis, to gain new insight into the link between fatty acid oxidation, amino acid metabolism and TCA cycle-related intermediate metabolites in liver and plasma. RESULTS: Rats treated with 3-thia fatty acids had 3-fold higher hepatic, but not adipose and skeletal muscle, expression of the thioesterase 3-hydroxyisobutyryl-CoA hydrolase (Hibch), which controls the formation of 3-hydroxyisobutyrate (3-HIB) in the valine degradation pathway. Consequently, 3-thia fatty acid-stimulated hepatic fatty acid oxidation and ketogenesis was accompanied by decreased plasma 3-HIB and increased methylmalonic acid (MMA) concentrations further downstream in BCAA catabolism. The higher plasma MMA corresponded to higher MMA-CoA hydrolase activity and hepatic expression of GTP-specific succinyl-CoA synthase (Suclg2) and succinate dehydrogenase (Sdhb), and lower MMA-CoA mutase activity. Plasma 3-HIB correlated positively to plasma and hepatic concentrations of TAG, plasma total fatty acids, plasma NEFA and insulin/glucose ratio, while the reverse correlations were seen for MMA. CONCLUSION: Our study provides new insight into TCA cycle-related metabolic changes associated with altered hepatic fatty acid flux, and identifies 3-HIB and MMA as novel circulating markers reflective of mitochondrial ß-oxidation in male Wistar rats.

A chicken protein hydrolysate exerts anti-atherosclerotic effect beyond plasma cholesterol-lowering activity in Apoe-/- mice.

Chicken protein hydrolysates (CPHs) generated from rest raw materials through enzymatic hydrolysis using Corolase PP or Alcalase were shown to reduce inflammation and stimulate hepatic mitochondrial fatty acid oxidation in high-fat-fed mice. This study investigates the effect of CPH diets in atherosclerosis-prone apolipoprotein E-deficient (Apoe-/-) mice. Apoe-/- mice were divided into three groups of 12 animals and fed high-fat diets with casein (control), Alcalase CPH, or Corolase PP CPH. After 12 weeks, mice were sacrificed, blood samples were collected, and aorta was dissected for subsequent én face analysis. Mice fed Corolase PP CPH but not Alcalase CPH had significantly lower % atherosclerotic plaque area in the aortic arch compared to controls (p = .015 and p = .077, respectively). Plasma and liver cholesterol and triacylglycerol remained constant, but levels of the fatty acid C20:5n-3 were increased, accompanied by an elevated delta-5 desaturase index in both CPHs groups. Moreover, a significant reduction of plasma MCP-1 was detected in Corolase PP CPH compared to control. Overall, our data show that protein hydrolysates from chicken reduced atherosclerosis and attenuated systemic risk factors related to atherosclerotic disorders, not related to changes in the level of plasma cholesterol.

Chicken Protein Hydrolysates Have Anti-Inflammatory Effects on High-Fat Diet Induced Obesity in Mice.

Background: Studies have shown that dietary source of protein and peptides can affect energy metabolism and influence obesity-associated diseases. This study aimed to investigate the impact of different chicken protein hydrolysates (CPHs) generated from chicken rest raw materials in a mouse obesity model. Methods: Male C57BL/6 mice were fed a high-fat, high-sucrose diet with casein or CPHs generated using Papain + Bromelain, Alcalase, Corolase PP, or Protamex for 12 weeks (n = 12). Body weight, feed intake, and intraperitoneal glucose tolerance was determined, and plasma and liver and adipose tissues were collected at sacrifice. Results: The average feed intake and body weight did not differ between the groups and white adipose tissue depots were unchanged, except for a reduction in the subcutaneous depot in mice fed the Protamex CPH diet. Moreover, the CPH diets did not prevent increased fasting glucose and insulin levels. Interestingly, the hepatic mitochondrial fatty acid ß-oxidation was increased in mice fed Alcalase and Corolase PP CPHs. All CPH diets reduced plasma interleukine (IL)-1ß, interferon-γ, tumor necrosis factor α, and monocyte chemotactic protein 1 compared to control, indicating anti-inflammatory effects. In addition, Corolase PP and Protamex CPHs significantly reduced plasma levels of IL-1α, IL-2, IL-6, IL-10, and granulocyte macrophage colony-stimulating factor. Conclusions: CPH diets were not able to counteract obesity and glucose intolerance in a mouse obesity model, but strongly reduced inflammatory parameters associated with obesity. Alcalase and Corolase PP CPHs also stimulated mitochondrial fatty acid ß-oxidation. The possibility that hydrolysates from chicken rest raw materials could alleviate obesity-associated metabolic disease should be investigated further.