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      Effects of Mealworm Fermentation Extract and Soy Protein Mix Ratio on Hepatic Glucose and Lipid Metabolism in Obese-Induced Mice

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          Abstract

          Previous studies found that mealworm fermentation extract (TMP) reduced alcoholic hepatic steatogenesis. This study examined how the ratio of TMP and soy protein (SP) mix affected glucose and lipid metabolism in obese mice given a high-fat diet (HFD). Mice were given HFD supplemented with 100% SP or the following three ratios of TMP and SP mix for 12 weeks: 20% (S4T1), 40% (S3T2), and 60% (S2T3) TMP. When compared to the SP group, the S2T3 group had considerably lower body weight gain and food consumption. When compared to the SP group, the S2T3 group had slightly lower blood insulin and leptin levels, as well as a lower homeostasis model assessment of insulin resistance score. The use of TMP instead of SP reduced the size of epididymal adipose tissue cells. An increase in the extent of substitution of SP with TMP inhibited the gene expression of hepatic fructolysis/gluconeogenesis ( KHK, ALDOB, DLD, and FBP1), lipogenesis ( FAS, SCD1, CD36, and DGAT2), and its transcriptional factors ( PPARγ and ChREBP). Furthermore, the S2T3 group dramatically reduced the expression of hepatic genes implicated in endoplasmic reticulum stress ( PDI) and antioxidant defense ( SOD1). The 60% TMP mix, in particular, reduced the expression of hepatic glucose and lipid metabolismrelated genes in HFD-fed mice. The manufacturing of functional processed goods may be accomplished by combining SP and TMP in a 2:3 ratio.

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          Most cited references37

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          Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis.

          The liver provides for long-term energy needs of the body by converting excess carbohydrate into fat for storage. Insulin is one factor that promotes hepatic lipogenesis, but there is increasing evidence that glucose also contributes to the coordinated regulation of carbohydrate and fat metabolism in liver by mechanisms that are independent of insulin. In this study, we show that the transcription factor, carbohydrate response element-binding protein (ChREBP), is required both for basal and carbohydrate-induced expression of several liver enzymes essential for coordinated control of glucose metabolism, fatty acid, and the synthesis of fatty acids and triglycerides in vivo.
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            Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials.

            It is currently unclear whether altering the carbohydrate-to-protein ratio of low-fat, energy-restricted diets augments weight loss and cardiometabolic risk markers. The objective was to conduct a systematic review and meta-analysis of studies that compared energy-restricted, isocaloric, high-protein, low-fat (HP) diets with standard-protein, low-fat (SP) diets on weight loss, body composition, resting energy expenditure (REE), satiety and appetite, and cardiometabolic risk factors. Systematic searches were conducted by using MEDLINE, EMBASE, PubMed, and the Cochrane Central Register of Controlled Trials to identify weight-loss trials that compared isocalorically prescribed diets matched for fat intake but that differed in protein and carbohydrate intakes in participants aged ≥18 y. Twenty-four trials that included 1063 individuals satisfied the inclusion criteria. Mean (±SD) diet duration was 12.1 ± 9.3 wk. Compared with an SP diet, an HP diet produced more favorable changes in weighted mean differences for reductions in body weight (-0.79 kg; 95% CI: -1.50, -0.08 kg), fat mass (FM; -0.87 kg; 95% CI: -1.26, -0.48 kg), and triglycerides (-0.23 mmol/L; 95% CI: -0.33, -0.12 mmol/L) and mitigation of reductions in fat-free mass (FFM; 0.43 kg; 95% CI: 0.09, 0.78 kg) and REE (595.5 kJ/d; 95% CI: 67.0, 1124.1 kJ/d). Changes in fasting plasma glucose, fasting insulin, blood pressure, and total, LDL, and HDL cholesterol were similar across dietary treatments (P ≥ 0.20). Greater satiety with HP was reported in 3 of 5 studies. Compared with an energy-restricted SP diet, an isocalorically prescribed HP diet provides modest benefits for reductions in body weight, FM, and triglycerides and for mitigating reductions in FFM and REE.
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              Increasing dietary leucine intake reduces diet-induced obesity and improves glucose and cholesterol metabolism in mice via multimechanisms.

              Leucine, as an essential amino acid and activator of mTOR (mammalian target of rapamycin), promotes protein synthesis and suppresses protein catabolism. However, the effect of leucine on overall glucose and energy metabolism remains unclear, and whether leucine has beneficial effects as a long-term dietary supplement has not been examined. In the present study, we doubled dietary leucine intake via leucine-containing drinking water in mice with free excess to either a rodent chow or a high-fat diet (HFD). While it produced no major metabolic effects in chow-fed mice, increasing leucine intake resulted in up to 32% reduction of weight gain (P < 0.05) and a 25% decrease in adiposity (P < 0.01) in HFD-fed mice. The reduction of adiposity resulted from increased resting energy expenditure associated with increased expression of uncoupling protein 3 in brown and white adipose tissues and in skeletal muscle, while food intake was not decreased. Increasing leucine intake also prevented HFD-induced hyperglycemia, which was associated with improved insulin sensitivity, decreased plasma concentrations of glucagon and glucogenic amino acids, and downregulation of hepatic glucose-6-phosphatase. Additionally, plasma levels of total and LDL cholesterol were decreased by 27% (P < 0.001) and 53% (P < 0.001), respectively, in leucine supplemented HFD-fed mice compared with the control mice fed the same diet. The reduction in cholesterol levels was largely independent of leucine-induced changes in adiposity. In conclusion, increases in dietary leucine intake substantially decrease diet-induced obesity, hyperglycemia, and hypercholesterolemia in mice with ad libitum consumption of HFD likely via multiple mechanisms.
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                Author and article information

                Journal
                Prev Nutr Food Sci
                Prev Nutr Food Sci
                Preventive Nutrition and Food Science
                The Korean Society of Food Science and Nutrition
                2287-1098
                2287-8602
                30 September 2023
                30 September 2023
                30 September 2023
                : 28
                : 3
                : 255-262
                Affiliations
                [1 ]Department of Agricultural Biology, National Institution of Agricultural Sciences, Rural Development Administration, Jeonbuk 55365, Korea
                [2 ]Department of Food and Nutrition, Sunchon National University, Jeonnam 57922, Korea
                Author notes
                Correspondence to Mi-Kyung Lee, E-mail: leemk@ 123456scnu.ac.kr
                Author information
                https://orcid.org/0000-0002-7313-0901
                https://orcid.org/0000-0002-6064-5295
                Article
                pnfs-28-3-255
                10.3746/pnf.2023.28.3.255
                10567600
                37842251
                6550d020-7282-4ddc-960f-88bd19202ebc
                Copyright © 2023 by The Korean Society of Food Science and Nutrition.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 March 2023
                : 30 May 2023
                : 20 June 2023
                Categories
                Original

                fatty liver,high-fat diet,lipid metabolism,soybean protein,tenebrio molitor

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