{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T03:30:31Z","timestamp":1783999831691,"version":"3.55.0"},"reference-count":49,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2018,2,23]],"date-time":"2018-02-23T00:00:00Z","timestamp":1519344000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Obesity-induced adipose inflammation has been demonstrated to be a key cause of insulin resistance. Peptides derived from bovine \u03b1-lactalbumin have been shown to inhibit the activities of dipeptidyl peptidase IV (DPP-IV) and angiotensin converting enzyme (ACE), scavenge 2,2\u2032-azinobis [3-ethylbenzothiazoline-6-sulfonate] (ABTS+) radical and stimulate glucagon-like peptide-2 secretion. In the present study, the effects of bovine \u03b1-lactalbumin hydrolysates (\u03b1-LAH) on adipose insulin resistance and inflammation induced by high-fat diet (HFD) were investigated. The insulin resistance model was established by feeding C57BL\/6J mice with HFD (60% kcal from fat) for eight weeks. Then, the mice were fed with HFD and bovine \u03b1-LAH of different doses (100 mg\/kg b.w., 200 mg\/kg b.w. and 400 mg\/kg b.w.) for another 12 weeks to evaluate its protective effects against HFD-induced insulin resistance. The oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (ipITT) were conducted after intervention with \u03b1-LAH for 10 weeks and 11 weeks, respectively. Results showed that bovine \u03b1-LAH significantly reduced body weight, blood glucose, serum insulin, and HOMA-IR (homeostatic model assessment of insulin resistance) levels, lowered the area-under-the-curve (AUC) during OGTT and ipITT, and downregulated inflammation-related gene [tumor necrosis factor (TNF)-\u03b1, interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1] expression in adipose tissues of HFD-fed C57BL\/6J mice. Furthermore, bovine \u03b1-LAH also suppressed insulin receptor substrate 1 (IRS-1) serine phosphorylation (Ser307, Ser612), enhanced protein kinase B (known as Akt) phosphorylation, and inhibited the activation of inhibitor of kappaB kinase (IKK) and mitogen activated protein kinase (MAPK) signaling pathways in adipose tissues of HFD-fed C57BL\/6J mice. These results suggested that bovine \u03b1-LAH could ameliorate adipose insulin resistance and inflammation through IKK and MAPK signaling pathways in HFD-fed C57BL\/6J mice.<\/jats:p>","DOI":"10.3390\/nu10020242","type":"journal-article","created":{"date-parts":[[2018,2,23]],"date-time":"2018-02-23T12:41:40Z","timestamp":1519389700000},"page":"242","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Bovine \u03b1-Lactalbumin Hydrolysates (\u03b1-LAH) Ameliorate Adipose Insulin Resistance and Inflammation in High-Fat Diet-Fed C57BL\/6J Mice"],"prefix":"10.3390","volume":"10","author":[{"given":"Jing","family":"Gao","sequence":"first","affiliation":[{"name":"Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science &amp; Nutritional Engineering, China Agricultural University, Beijing 100083, China"},{"name":"College of Food Science and Nutritional Engineering, Key Laboratory of Functional Dairy, Ministry of Education, China Agricultural University, Beijing 100083, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiajia","family":"Song","sequence":"additional","affiliation":[{"name":"Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science &amp; Nutritional Engineering, China Agricultural University, Beijing 100083, China"},{"name":"College of Food Science and Nutritional Engineering, Key Laboratory of Functional Dairy, Ministry of Education, China Agricultural University, Beijing 100083, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueying","family":"Mao","sequence":"additional","affiliation":[{"name":"Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science &amp; Nutritional Engineering, China Agricultural University, Beijing 100083, China"},{"name":"College of Food Science and Nutritional Engineering, Key Laboratory of Functional Dairy, Ministry of Education, China Agricultural University, Beijing 100083, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2018,2,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"2033","DOI":"10.1007\/s00125-017-4341-0","article-title":"Deficiency in plasmacytoid dendritic cells and type I interferon signalling prevents diet-induced obesity and insulin resistance in mice","volume":"60","author":"Hannibal","year":"2017","journal-title":"Diabetologia"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1218","DOI":"10.3390\/nu5041218","article-title":"Dyslipidemia in obesity: Mechanisms and potential targets","volume":"5","author":"Klop","year":"2013","journal-title":"Nutrients"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"6184","DOI":"10.3390\/ijms15046184","article-title":"Obesity and its metabolic complications: The role of adipokines and the relationship between obesity, inflammation, insulin resistance, dyslipidemia and nonalcoholic fatty liver disease","volume":"15","author":"Jung","year":"2014","journal-title":"Int. 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