Chickpea (Cicer arietinum) protein hydrolysate ameliorates the metabolic effect of feeding a high-fat-diet-induced obesity in mice by modulating inflammation

Radlowski, Casey John

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https://hdl.handle.net/2142/116123 Copy

Description

Title

Chickpea (Cicer arietinum) protein hydrolysate ameliorates the metabolic effect of feeding a high-fat-diet-induced obesity in mice by modulating inflammation

Author(s)

Radlowski, Casey John

Issue Date

2022-07-21

Director of Research (if dissertation) or Advisor (if thesis)

DeMejia, Elvira

Committee Member(s)

• Chapman-Novakofski, Karen
• Amengual Terrasa, Jaume

Department of Study

Food Science & Human Nutrition

Discipline

Food Science & Human Nutrition

Degree Granting Institution

University of Illinois at Urbana-Champaign

Degree Name

M.S.

Degree Level

Thesis

Keyword(s)

• Obesity
• Chickpea (Cicer Arietinum)
• Type 2 Diabetes
• Mouse
• High fat diet

Abstract

Obesity is a growing epidemic in the United States with over 40% of the country suffering from this disease. Obesity increases the risk of many chronic conditions,such as type 2 diabetes (T2D). Foods that are high in nutrients and low in calories, such as chickpeas, can help treat obesity. While whole chickpeas assist in weight loss, chickpea protein can also aid in managing T2D as it contains several bioactive peptides that might influence glucose absorption. The aim of this study was to evaluate the efficacy of a chickpea protein hydrolysate (CPH) to ameliorate markers of obesity in a 16-week mouse model of metabolic dysfunction when fed a high fat diet (HFD). Additionally, liver tissue was analyzed for evidence of non alcoholic fatty liver disease (NAFLD). CPH was produced by an alcalase and Flavourzyme®️ dual-system. The hydrolysate was characterized by LC-MSMS to detect for anti-diabetic peptides. Fifty-two six-week-old male C57BL/6J mice (n = 13/group) were randomized: standard diet (SD), HFD, HFD + 400 mg CPH/kg body weight (BW) (400 CPH), and HFD + 800 mg CPH/kg BW (800 CPH). CPH was administered daily to the treatment groups for the duration of the study. At the end of the study, plasma was analyzed for concentration of adiponectin, resistin, insulin, triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and inflammatory proteins. Feces were also collected and measured for amino acid and fatty acid concentrations. Adipose tissue underwent histological analysisfor adipocyte area and macrophage clustering. Liver was scored for NAFLD progression. Genes related to insulin resistance were also analyzed in adipose and liver. Three peptides in the hydrolysate were identified having angiotensin-converting enzyme (ACE)-inhibitory and dipeptidyl peptidase-IV (DPP-IV) inhibitory properties. After the 16-week study, weight gain for 800 CPH was lower (19.2%, p < 0.01) than HFD control. Plasma insulin concentration was highest (87.57 ± 58.6 µIU/mL, p < 0.05) for 800 CPH amongst all groups. For triglycerides, a significant difference (p < 0.05) was only found between 800 CPH (75.13 ± 27.45 mg/dL) and 400 CPH (46.22 ± 13.63 mg/dL). SD control had significantly (p < 0.05) lower total cholesterol and LDL concentrations than all HFD groups, but no differences were found for HDL among all groups. The 400 CPH group had reduced (p < 0.05) plasma levels of interleukin (IL)-1α, C-X-C motif chemokine 5 (LIX) lymphotactin, monocyte chemoattractant protein (MCP)-1, macrophage-colony stimulating factor (MCSF), macrophage inflammatory protein (MIP)-1γ, chemokine ligand-1 (TCA-3), soluble tumor necrosis factor receptor I (sTNF RI) compared to HFD control while 800 CPH had reduced (p < 0.05) levels of IL-1 α and LIX compared to HFD control. Metabolomics analysisidentified an increase of fatty acids in feces for 800 CPH vs HFD control. Adipocyte area was significantly smaller (2342 ± 647 µm2) for SD control than all HFD groups. Macrophage infiltration of adipocytes analysis revealed that 800 CPH had lower clustering than 400 CPH (6.5 ± 3.7 mm2 vs 17.8 ± 14.1 mm2, respectively). NAFLD scoring showed significant (p < 0.05) delineation between each group; HFD control: 5.1 ± 0.6, 400 CPH: 3.6 ± 0.8, 800 CPH: 1.2 ± 0.4, and SD control: 0.3 ± 0.2. Gene expression analysis of adipose determined SD control had upregulation (FC > 2) of genes related to carbohydrate (Gys1, Pck1, Pdk2) and lipid (Fasn, Pparg) metabolism compared to HFD control, while 800 CPH had upregulation of genes for inflammation (Il1β and Il18R1) and carbohydrate metabolism (Hk2) compared to HFD control. In liver, SD control had upregulation of genes for lipid metabolism (Acaca, Acacb, Acsl4, Cebpa, Lepr) compared HFD control while 400 CPH had downregulated genes related to adipokine (Tnfrsf1b) and insulin signaling (Pik3r1, Ikbkb, Map2k1) compared to HFD control.

Graduation Semester

2022-08

Type of Resource

Thesis

Copyright and License Information

Copyright 2022 Casey Radlowski

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