High saturated fat and low carbohydrate diet decreases lifespan independent of body weight in mice

Müller, Alexandre Pastoris; Dietrich, Marcelo O.; Assis, Adriano Martimbianco de; Souza, Diogo Onofre Gomes de; Portela, Luis Valmor Cruz

doi:10.1186/2046-2395-2-10

Cited by 15 publications

(11 citation statements)

References 26 publications

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“…Muller and colleagues found similarly that male C57BL/6 mice fed a high fat diet (60% energy from saturated and unsaturated fats) for 27 months were either diet-resistant or developed diet-induced obesity related to body weight gain, and had decreased life expectancy compared to the chow-fed mice. However, the survival rate was not different among the two groups; indicating that a high fat diet decreases survival rate independent of body weight gain (Muller et al, 2013a). This is also shown to be true in BFMI860 mice where feeding a high fat diet showed an increased risk of mortality, but body weight itself had a marginal effect on lifespan within the group of mice on high fat diet (Wagener et al, 2013).…”

Section: Discussionmentioning

confidence: 69%

“…However, consumption of high levels of corn oil rich in poly-and monounsaturated fats (58.6% fat-derived calories) in C57BL/6 male mice has been shown to improve health and longevity, provided that total calorie consumption stays within normal bounds (Si et al, 2014). Muller and colleagues report that C57BL/6 male mice fed a high fat diet (60% energy from saturated and unsaturated fat-45% lard and 15% soybean oil) for over two years have decreased life expectancy independent of body weight gain (Muller et al, 2013b). Similarly, the initiation of a HFD in middle-aged mice has a detrimental impact on general health and survival (Baur et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Gene-by-environmental modulation of longevity and weight gain in the murine BXD family

Roy

Sleiman

Jha

et al. 2019

Preprint

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Diet and environmental factors profoundly modulate lifespan. We measured longevity as a function of diet, and weight gain across a large genetically diverse BXD cohort which segregates for over 6 million variants, making it ideal for the analysis of gene-by-diet interactions that modulate lifespan. We followed 1348 females from parental strains, C57BL/6J and DBA/2J, and 76 BXD progeny strains on a standard low fat diet (CD, 18% calories from fat) or a widely used high fat diet (HFD, 60% calories from fat) across their natural life span. A diet rich in saturated fats shortens lifespan by an average of 85 days (HFD 605 ± 6, n = 685; CD 690 ± 8, n = 663), roughly equivalent to a 7-year decrease in humans. This diet is associated with an average two-fold higher age-adjusted risk of death compared to CD. Individual strains show remarkably wide variation in responses to diet, ranging from -54% on HFD in BXD65 to +37% on HFD in BXD8.Baseline weight and early weight gain on HFD associates negatively with longevity, with a gram increase causing lifespan to decrease by 4 days. By 500 days of age, BXDs on HFD gained 4X more weight than those on CD. However, strain-specific variation in the change in body weight does not significantly correlate with strain-specific life span. Major morbidities appear to be influenced by diet, with cases on HFD showing increased prevalence and severity of cardiovascular disease and lesions. Overall, we find that diet significantly impacts longevity even after adjusting for weight gain.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Gene-by-environmental modulation of longevity and weight gain in the murine BXD family

Roy

Sleiman

Jha

et al. 2019

Preprint

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“…Immediately after an i.p. injection of glucose solution (2 mg/g body weight), the blood glucose levels were evaluated at 30, 90, and 120 min [Muller et al, ]. Glucose was measured with a glucosimeter (AccuChek Active, Roche Diagnostics®, São Paulo, Brazil).…”

Section: Methodsmentioning

confidence: 99%

Prior Exercise Training Prevent Hyperglycemia in STZ Mice by Increasing Hepatic Glycogen and Mitochondrial Function on Skeletal Muscle

Carvalho

Silva

Serafini

et al. 2016

J of Cellular Biochemistry

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Diabetes mellitus is a metabolic disorder characterized by hyperglycemia. We investigated the effect of a prior 30 days voluntary exercise protocol on STZ-diabetic CF1 mice. Glycemia, and the liver and skeletal muscle glycogen, mitochondrial function, and redox status were analyzed up to 5 days after STZ injection. Animals were engaged in the following groups: Sedentary vehicle (Sed Veh), Sedentary STZ (Sed STZ), Exercise Vehicle (Ex Veh), and Exercise STZ (Ex STZ). Exercise prevented fasting hyperglycemia in the Ex STZ group. In the liver, there was decreased on glycogen level in Sed STZ group but not in EX STZ group. STZ groups showed decreased mitochondrial oxygen consumption compared to vehicle groups, whereas mitochondrial H O production was not different between groups. Addition of ADP to the medium did not decrease H O production in Sed STZ mice. Exercise increased GSH level. Sed STZ group increased nitrite levels compared to other groups. In quadriceps muscle, glycogen level was similar between groups. The Sed STZ group displayed decreased O consumption, and exercise prevented this reduction. The H O production was higher in Ex STZ when compared to other groups. Also, GSH level decreased whereas nitrite levels increased in the Sed STZ compared to other groups. The PGC1 α levels increased in Sed STZ, Ex Veh, and Ex STZ groups. In summary, prior exercise training prevents hyperglycemia in STZ-mice diabetic associated with increased liver glycogen storage, and oxygen consumption by the mitochondria of skeletal muscle implying in increased oxidative/biogenesis capacity, and improved redox status of both tissues. J. Cell. Biochem. 118: 678-685, 2017. © 2016 Wiley Periodicals, Inc.

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“…The lack of Sod1 further exacerbates the accumulation of oxidative damage both in high fat feeding and aging whereas overexpression of Sod2 prevents oxidative damage in both cases (FIGURE 2). While lifespan of high fat-fed antioxidant mutant mice has not been determined under these conditions, other reports suggest that a high fat diet moderately diminishes mouse lifespan without significantly altering the incidence of uncommon fatal rodent pathologies (127, 128). Thus, this feeding protocol might be a solution to deliver a robust, chronic oxidative stress in a controlled manner.…”

Section: Possible Conclusion 3: There Are Still Too Many Poorly Answementioning

confidence: 99%

Revisiting an age-old question regarding oxidative stress

Edrey

Salmon

2014

Free Radical Biology and Medicine

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Significant advances in maintaining health throughout life can be made through a clear understanding of the fundamental mechanisms that regulate aging. The Oxidative Stress Theory of Aging (OSTA) is likely the most well-studied mechanistic theory of aging and suggests that the rate of aging is controlled by accumulation of oxidative damage. To directly test the OSTA, aging has been measured in several lines of mice with genetic alteration of the expression of enzymatic antioxidants. Under its strictest interpretation, these studies do not support the OSTA, as modulation of antioxidant expression does not generally affect mouse lifespan. However, the incidence of many age-related diseases and pathologies is altered in these models suggesting that oxidative stress does significantly impact some aspects of the aging process. Further, oxidative stress may affect aging in disparate patterns among tissues or under different environmental conditions. In this review, we summarize the current literature regarding aging in antioxidant mutant mice and offer several interpretations on their support of the OSTA.

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High saturated fat and low carbohydrate diet decreases lifespan independent of body weight in mice

Cited by 15 publications

References 26 publications

Gene-by-environmental modulation of longevity and weight gain in the murine BXD family

Gene-by-environmental modulation of longevity and weight gain in the murine BXD family

Prior Exercise Training Prevent Hyperglycemia in STZ Mice by Increasing Hepatic Glycogen and Mitochondrial Function on Skeletal Muscle

Revisiting an age-old question regarding oxidative stress

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