Dietary protein restriction induces steatohepatitis and alters leptin/signal transducers and activators of transcription 3 signaling in lactating rats

Kwon, Duk-Hwa; Kang, Woo Dae; Nam, Yoon Seok; Lee, Mi‐Sun; Lee, In Young; Kim, Hye Joung; Rajasekar, Periyannan; Lee, Jae-Hyuk; Baik, Myunggi

doi:10.1016/j.jnutbio.2011.04.002

Cited by 24 publications

(16 citation statements)

References 32 publications

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“…Higher incidence of fatty liver is found in non-pregnant humans and laboratory animals with dietary protein deficiency [40] or high fructose consumption [41, 42]. Severe fatty infiltration has been demonstrated with low protein intake during lactation [43]. The data reported here extend those observations to indicate that the impact of low protein feeding is more severe in the lactating state compared with non-pregnant animals.…”

Section: Discussionsupporting

confidence: 70%

Fructose consumption during pregnancy and lactation induces fatty liver and glucose intolerance in rats

Zou¹,

Arentson²,

Teegarden³

et al. 2012

Nutrition Research

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Nutritional insults during pregnancy and lactation are health risks for mother and offspring. Both fructose and low protein diets are linked to hepatic steatosis and insulin resistance in non-pregnant animals. We hypothesized that dietary fructose or low protein intake during pregnancy may exacerbate the already compromised glucose homeostasis to induce gestational diabetes and fatty liver. Therefore, we investigated and compared the effects of low protein or fructose intake on hepatic steatosis and insulin resistance in unmated controls and pregnant and lactating rats. Sprague-Dawley rats were fed either a control (CT), a 63% fructose (FR) or an 8% protein (LP) diet. Glucose tolerance test at day 17 of the study revealed greater (P < 0.05) blood glucose at 10 (75.6 vs. 64.0 ± 4.8 mg/dl) and 20 (72.4 vs. 58.6 ± 4.0 mg/dl) min after glucose dose and greater area under the curve (4302.3 vs. 3763.4 ± 263.6 mg·dl−1·min−1) for FR-fed dams compared with CT-fed dams. The rats were euthanized at 21 days postpartum. Both the FR- and LP-fed dams had enlarged (P < 0.05) livers (9.3, 7.1 vs. 4.8 ± 0.2 % body weight) and elevated (P < 0.05) liver triacylglycerol (216.0, 130.0 vs. 19.9 ± 12.6 mg/g liver weight) compared with CT-fed dams. FR induced fatty liver and glucose intolerance in pregnant and lactating rats, but not unmated control rats. The data demonstrate a unique physiological status response to diet resulting in the development of gestational diabetes coupled with hepatic steatosis in FR-fed dams, which is more severe than a LP diet.

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Section: Discussionsupporting

confidence: 70%

Fructose consumption during pregnancy and lactation induces fatty liver and glucose intolerance in rats

Zou¹,

Arentson²,

Teegarden³

et al. 2012

Nutrition Research

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“…Hepatic lipid accumulation drives many of the negative metabolic effects of diet‐induced obesity, including hepatic insulin resistance. There is conflicting information on how dietary protein and methionine affect the accumulation of hepatic lipids, with some studies showing that MR protects against fatty liver disease (14, 15), and other studies showing that a diet deficient in both methionine and choline induces hepatic steatosis (34, 35). We therefore examined hepatic steatosis in MD mice fed a WD.…”

Section: Resultsmentioning

confidence: 99%

Short‐term methionine deprivation improves metabolic health via sexually dimorphic, mTORCI‐independent mechanisms

Yang

Miller

et al. 2018

FASEB j.

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Obesity and diabetes are major challenges to global health, and there is an urgent need for interventions that promote weight loss. Dietary restriction of methionine promotes leanness and improves metabolic health in mice and humans. However, poor long-term adherence to this diet limits its translational potential. In this study, we develop a short-term methionine deprivation (MD) regimen that preferentially reduces fat mass, restoring normal body weight and glycemic control to diet-induced obese mice of both sexes. The benefits of MD do not accrue from calorie restriction, but instead result from increased energy expenditure. MD promotes increased energy expenditure in a sex-specific manner, inducing the fibroblast growth factor (Fgf)-21-uncoupling protein (Ucp)-1 axis only in males. Methionine is an agonist of the protein kinase mechanistic target of rapamycin complex (mTORC)-1, which has been proposed to play a key role in the metabolic response to amino acid-restricted diets. In our study, we used a mouse model of constitutive hepatic mTORC1 activity and demonstrate that suppression of hepatic mTORC1 signaling is not required for the metabolic effects of MD. Our study sheds new light on the mechanisms by which dietary methionine regulates metabolic health and demonstrates the translational potential of MD for the treatment of obesity and type 2 diabetes.-Yu, D., Yang, S. E., Miller, B. R., Wisinski, J. A., Sherman, D. S., Brinkman, J. A., Tomasiewicz, J. L., Cummings, N. E., Kimple, M. E., Cryns, V. L., Lamming, D. W. Short-term methionine deprivation improves metabolic health via sexually dimorphic, mTORC1-independent mechanisms.

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“…Maternal food intake during lactation also affects permanent changes in the nutritional and hormonal statuses of the offspring [7]. Changes in satiety signals by maternal malnutrition may affect energy intake or metabolic rate throughout the offspring’s lifetime and have the potential to induce an overweight state and hepatic steatosis in rat offspring [8,9,10]. Although maternal malnutrition is a major factor adversely affecting foetal and neonatal growth and development, with lifelong consequences, the underlying molecular mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Maternal Food Restriction during Pregnancy and Lactation Adversely Affect Hepatic Growth and Lipid Metabolism in Three-Week-Old Rat Offspring

Lee

You

Kwon

et al. 2016

IJMS

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Maternal malnutrition influences the early development of foetal adaptive changes for survival. We explored the effects of maternal undernutrition during gestation and lactation on hepatic growth and function. Sprague-Dawley rats were fed a normal or a food-restricted (FR) diet during gestation and/or lactation. We performed analyses of covariance (adjusting for the liver weight/body weight ratio) to compare hepatic growth and lipid metabolism among the offspring. Maternal FR during gestation triggered the development of wide spaces between hepatic cells and increased the expression of mammalian target of rapamycin (mTOR) in three-week-old male offspring compared with controls (both p < 0.05). Offspring nursed by FR dams exhibited wider spaces between hepatic cells and a lower liver weight/body weight ratio than control offspring, and increased mTOR expression (p < 0.05). Interestingly, the significant decrease in expression of lipogenic-related genes was dependent on carbohydrate-responsive element-binding protein, despite the increased expression of sterol regulatory element-binding protein 1 (SREBP1) (p < 0.05). This study demonstrated increased expression of key metabolic regulators (mTOR and SREBP1), alterations in lipid metabolism, and deficits in hepatic growth in the offspring of FR-treated dams.

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Dietary protein restriction induces steatohepatitis and alters leptin/signal transducers and activators of transcription 3 signaling in lactating rats

Cited by 24 publications

References 32 publications

Fructose consumption during pregnancy and lactation induces fatty liver and glucose intolerance in rats

Fructose consumption during pregnancy and lactation induces fatty liver and glucose intolerance in rats

Short‐term methionine deprivation improves metabolic health via sexually dimorphic, mTORCI‐independent mechanisms

Maternal Food Restriction during Pregnancy and Lactation Adversely Affect Hepatic Growth and Lipid Metabolism in Three-Week-Old Rat Offspring

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