scholarly journals Diet composition influences the metabolic benefits of short cycles of very low caloric intake

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alberto Diaz-Ruiz ◽  
Tyler Rhinesmith ◽  
Laura C. D. Pomatto-Watson ◽  
Nathan L. Price ◽  
Farzin Eshaghi ◽  
...  
Keyword(s):  
Diet Composition ◽  
Caloric Intake ◽  
Calorie Intake ◽  
Metabolic Memory ◽  
Metabolic Flexibility ◽  
Standard Laboratory ◽  
Male Mice ◽  
Diet Induced Obesity ◽  
Obesogenic Diet ◽  
The Impact

AbstractDiet composition, calories, and fasting times contribute to the maintenance of health. However, the impact of very low-calorie intake (VLCI) achieved with either standard laboratory chow (SD) or a plant-based fasting mimicking diet (FMD) is not fully understood. Here, using middle-aged male mice we show that 5 months of short 4:10 VLCI cycles lead to decreases in both fat and lean mass, accompanied by improved physical performance and glucoregulation, and greater metabolic flexibility independent of diet composition. A long-lasting metabolomic reprograming in serum and liver is observed in mice on VLCI cycles with SD, but not FMD. Further, when challenged with an obesogenic diet, cycles of VLCI do not prevent diet-induced obesity nor do they elicit a long-lasting metabolic memory, despite achieving modest metabolic flexibility. Our results highlight the importance of diet composition in mediating the metabolic benefits of short cycles of VLCI.

Macronutrients and fibre requirements during pregnancy

2015 ◽  
Author(s):  
Sir Peter Gluckman ◽  
Mark Hanson ◽  
Chong Yap Seng ◽  
Anne Bardsley
Keyword(s):  
Fetal Development ◽  
Blood Glucose Concentration ◽  
Maternal Diet ◽  
Calorie Intake ◽  
Food Component ◽  
Glucose Levels ◽  
Embryonic And Fetal Development ◽  
Diet Induced Obesity ◽  
Total Body ◽  
The Impact

In this chapter, the impact of varying intakes of protein, carbohydrate and lipids, which are the key nutrients that contribute to calorie intake, is examined. Fibre is also an important food component that needs to be considered. The maternal macronutrient profile can influence embryonic and fetal development. For instance, both low and excessively high protein intakes during pregnancy are associated with restricted growth, increased adiposity, and impaired glucose tolerance. High-fat maternal diets can significantly increase the susceptibility to diet-induced obesity and percentage total body fat in offspring, although types of fats need to be considered, as intake of polyunsaturated fatty acids is important for fetal development. The type and content of carbohydrate (high- vs low-glycaemic sources) in the maternal diet influences blood glucose concentration, which has a direct effect on fetal glucose levels and metabolism.

Knockout of nephron ATP6AP2 impairs proximal tubule function and prevents high fat diet induced obesity in male mice

Endocrinology ◽  
2021 ◽  
Author(s):  
Silas A Culver ◽  
Safia Akhtar ◽  
Callie Rountree-Jablin ◽  
Susanna R Keller ◽  
Helen P Cathro ◽  
...  
Keyword(s):  
Body Weight ◽  
Proximal Tubule ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Caloric Intake ◽  
Normal Diet ◽  
Male Mice ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Urinary Glucose

Abstract ATP6AP2 expression is increased in the nephron during high fat diet (HFD) and its knockout (ATP6AP2 KO) reduces body weight (WT) in mice. We evaluated the contribution of ATP6AP2 to urinary glucose (UG) and albumin (Ualb) handling during HFD. We hypothesized that nephron ATP6AP2 KO increases UG and Ualb and minimizes HFD-induced obesity. Eight-week old male C57BL/6J mice with inducible nephron specific ATP6AP2 KO and non-induced controls (C) were fed either normal diet (ND, 12% kcal fat) or HFD (45% kcal fat) for 6 months. ATP6AP2 KO mice on ND had 20% (p<0.01) lower WT compared to C. HFD fed mice had 41% (p<0.05) greater WT than ND fed C. In contrast, ATP6AP2 KO abrogated the increase in WT induced by HFD by 40% (p<0.05). Mice on HFD had less caloric intake compared to ND controls (p<0.01). There were no significant differences in metabolic rate between all groups. UG and Ualb was significantly increased in ATP6AP2 KO mice on both ND and HFD. ATP6AP2 KO showed greater levels of proximal tubule apoptosis and histologic evidence of proximal tubule injury. In conclusion, our results demonstrate that nephron specific ATP6AP2 KO is associated with glucosuria and albuminuria, most likely secondary to renal proximal tubule injury and/or dysfunction. Urinary loss of nutrients may have contributed to the reduced WT of knockout mice on ND and lack of WT gain in response to HFD. Future investigation should elucidate the mechanisms by which loss of renal ATP6AP2 causes proximal tubule injury and dysfunction.

Glutaredoxin1 knockout promotes high-fat diet-induced obesity in male mice but not in female ones

2021 ◽  
Author(s):  
Xiao yu Zou ◽  
Muhammad Ijaz Ahmad ◽  
Di Zhao ◽  
Min Zhang ◽  
Chunbao Li
Keyword(s):  
High Fat Diet ◽  
Calorie Intake ◽  
Male Mice ◽  
High Fat ◽  
Male And Female ◽  
Female Mice ◽  
Diet Induced Obesity

This study aims to explore how high-fat diet and glutaredoxin1 (Glrx1) deficiency affect the development of obesity in male and female mice. High-fat diet induced great differences in calorie intake...

Effect of replacing sardine oil with margarine on dyslipidemia, dysglycemia and redox status of adipose tissue in high-fat diet-induced obesity in Wistar rats

2017 ◽  
Vol 47 (1) ◽  
pp. 2-17 ◽  
Author(s):  
Sherazed Hamza-Reguig ◽  
Nabila Boukhari Benahmed Daidj ◽  
Sabrine Louala ◽  
Ahmed Boualga ◽  
Myriem Lamri-Senhadji
Keyword(s):  
Adipose Tissue ◽  
Glycosylated Hemoglobin ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
Content Type ◽  
Sardine Oil ◽  
Diet Induced Obesity ◽  
Obesogenic Diet ◽  
Cardiometabolic Risk Markers ◽  
The Impact

Purpose The purpose of this study was to investigate the impact of replacing two different fats on dyslipidemia, glycemic balance and adipose tissue redox status in obese rats. Design/methodology/approach Obesity was induced by feeding a high-mutton-fat diet during three months. An experimental group (n = 24) was divided into two groups that were fed during one month, 20 per cent of margarine or sardine oil. At Day 30, six rats from each group were sacrificed and the remaining rats were then subjected to a change in diet for one month: margarine was replaced by sardine oil and inversely, and then the rats were sacrificed. Three other groups (n = 6), each fed during two months, 20 per cent of margarine, sardine oil or mutton fat, served as controls. Findings Substitution of sardine oil by margarine compared to control sardine oil had increased triacylglycerols (TGs), glycosylated hemoglobin (HbA1c) and isoprostanes (IsoPs) values, but decreased thiobarbituric acid reactive substances (TBARS) and superoxide dismutase activity. Replacing margarine by sardine oil compared to control margarine reduced total cholesterol, TG, HbA1c, TBARS and IsoP contents but enhanced glutathione reductase and peroxidase activities. Nevertheless, comparing with the mutton fat, the two substitutions had improved glycemic and lipidic abnormalities and attenuated lipoperoxidation by enhancing enzymatic antioxidant defense. These favorable effects were better when margarine was replaced by sardine oil. Originality/value Substituting margarine with sardine oil seems to attenuate beneficial cardiometabolic risk markers associated to obesity and potentiate efficiency adipose tissue against the oxidative stress induced by the obesogenic diet.

scholarly journals A BAFF/APRIL axis regulates obesogenic diet-driven weight gain

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Calvin C. Chan ◽  
Isaac T. W. Harley ◽  
Paul T. Pfluger ◽  
Aurelien Trompette ◽  
Traci E. Stankiewicz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Negative Regulator ◽  
Brown Adipocyte ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Obesogenic Diet ◽  
Log Linear ◽  
The Impact

AbstractThe impact of immune mediators on weight homeostasis remains underdefined. Interrogation of resistance to diet-induced obesity in mice lacking a negative regulator of Toll-like receptor signaling serendipitously uncovered a role for B cell activating factor (BAFF). Here we show that overexpression of BAFF in multiple mouse models associates with protection from weight gain, approximating a log-linear dose response relation to BAFF concentrations. Gene expression analysis of BAFF-stimulated subcutaneous white adipocytes unveils upregulation of lipid metabolism pathways, with BAFF inducing white adipose tissue (WAT) lipolysis. Brown adipose tissue (BAT) from BAFF-overexpressing mice exhibits increased Ucp1 expression and BAFF promotes brown adipocyte respiration and in vivo energy expenditure. A proliferation-inducing ligand (APRIL), a BAFF homolog, similarly modulates WAT and BAT lipid handling. Genetic deletion of both BAFF and APRIL augments diet-induced obesity. Lastly, BAFF/APRIL effects are conserved in human adipocytes and higher BAFF/APRIL levels correlate with greater BMI decrease after bariatric surgery. Together, the BAFF/APRIL axis is a multifaceted immune regulator of weight gain and adipose tissue function.

scholarly journals Absence of muricholic acid due to Cyp2c-deficiency protects against high fat diet-induced obesity in male mice but promotes liver damage

2021 ◽  
Author(s):  
Antwi-Boasiako Oteng ◽  
Sei Higuchi ◽  
Alexander S. Banks ◽  
Rebecca A. Haeusler
Keyword(s):  
Liver Damage ◽  
High Fat Diet ◽  
Energy Content ◽  
Lipid Absorption ◽  
Chow Diet ◽  
Male Mice ◽  
Wild Type ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesogenic Diet

Objective: Murine-specific muricholic acids (MCAs) are reported to protect against obesity and associated metabolic disorders. However, the response of mice with genetic depletion of MCA to an obesogenic diet has not been evaluated. We used Cyp2c-deficient (Cyp2c-/-) mice, which lack MCAs and thus have a human-like bile acid (BA) profile, to directly investigate the potential role of MCAs in diet-induced obesity. Methods: Male and female Cyp2c-/- mice and wild-type controls were fed a standard chow diet or a high fat diet (HFD) for 18 weeks. We measured BA composition from a pool of liver, gallbladder, and intestine, as well as weekly body weight, food intake, lean and fat mass, systemic glucose homeostasis, energy expenditure, intestinal lipid absorption, fecal lipid, and energy content. Results: Cyp2c deficiency depleted MCAs and caused other changes in BA composition, namely a decrease in the ratio of 12α-hydroxylated (12α-OH) BAs to non-12α-OH BAs, without altering the total BA levels. While wild-type male mice became obese after HFD-feeding, Cyp2c-/- male mice were protected from obesity and associated metabolic dysfunctions. Cyp2c-/- male mice also showed reduced intestinal lipid absorption and increased lipid excretion, which was reversed by oral gavage with the 12α-OH BA, taurocholic acid. Cyp2c-/- mice also showed increased liver damage, which appeared stronger in females. Conclusion: MCA does not protect against diet-induced obesity but may protect against liver injury. Reduced lipid absorption in Cyp2c-deficient male mice is potentially due to a reduced ratio of 12α-OH/non-12α-OH BAs.

Does Impulsive Response to Internal and External Food Cues Lead to Higher Calorie Intake?

2018 ◽  
Vol 7 (1) ◽  
pp. 14-34
Author(s):  
Jebaraj Asirvatham
Keyword(s):  
Experimental Studies ◽  
Caloric Intake ◽  
Self Control ◽  
Calorie Intake ◽  
Food Cues ◽  
Behavioral Measures ◽  
Environmental Pressures ◽  
Impulsive Response ◽  
The Impact ◽  
The Relationship

Measuring the impact of self-control on caloric intake has proved challenging in non-experimental studies. In this article, we study the relationship between self-control and food intake quantified by calories. Using validated behavioral measures, we find that impulsivity increases caloric intake, and that restraint decreases intake. Furthermore, the effect of impulsivity and restraint is more pronounced at the upper end of the calorie distribution. Thus, individuals already consuming more calories display a heightened reaction and likelihood to succumb to food environmental pressures. An individual's decision to diet, when allowed to vary with behavioral measures, bears no unique significance on caloric intake. Our results are robust to different levels of physical activity and generally robust to underreporting.

scholarly journals Inheritable testicular metabolic memory of high-fat diet causes transgenerational sperm defects in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Luís Crisóstomo ◽  
Ivana Jarak ◽  
Luís P. Rato ◽  
João F. Raposo ◽  
Rachel L. Batterham ◽  
...  
Keyword(s):  
Sperm Quality ◽  
Feeding Habits ◽  
Reproductive Function ◽  
Principal Component ◽  
Testicular Tissue ◽  
Sperm Parameters ◽  
Metabolic Memory ◽  
High Fat ◽  
And Function ◽  
The Impact

AbstractThe consumption of energy-dense diets has contributed to an increase in the prevalence of obesity and its comorbidities worldwide. The adoption of unhealthy feeding habits often occurs at early age, prompting the early onset of metabolic disease with unknown consequences for reproductive function later in life. Recently, evidence has emerged regarding the intergenerational and transgenerational effects of high-fat diets (HFD) on sperm parameters and testicular metabolism. Hereby, we study the impact of high-fat feeding male mice (F0) on the testicular metabolome and function of their sons (F1) and grandsons (F2). Testicular content of metabolites related to insulin resistance, cell membrane remodeling, nutritional support and antioxidative stress (leucine, acetate, glycine, glutamine, inosine) were altered in sons and grandsons of mice fed with HFD, comparing to descendants of chow-fed mice. Sperm counts were lower in the grandsons of mice fed with HFD, even if transient. Sperm quality was correlated to testicular metabolite content in all generations. Principal Component Analysis of sperm parameters and testicular metabolites revealed an HFD-related phenotype, especially in the diet-challenged generation and their grandsons. Ancestral HFD, even if transient, causes transgenerational “inherited metabolic memory” in the testicular tissue, characterized by changes in testicular metabolome and function.

scholarly journals Metabolic Benefit of Chronic Caloric Restriction and Activation of Hypothalamic AGRP/NPY Neurons in Male Mice Is Independent of Ghrelin

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1430-1442 ◽  
Author(s):  
Nicole H. Rogers ◽  
Heidi Walsh ◽  
Oscar Alvarez-Garcia ◽  
Seongjoon Park ◽  
Bruce Gaylinn ◽  
...  
Keyword(s):  
Food Intake ◽  
Caloric Restriction ◽  
Liver Steatosis ◽  
Severe Hypoglycemia ◽  
Metabolic Flexibility ◽  
Male Mice ◽  
Ambulatory Activity ◽  
Ghrelin Receptor ◽  
Liver Gene ◽  
Acyl Ghrelin

Abstract Aging is associated with attenuated ghrelin signaling. During aging, chronic caloric restriction (CR) produces health benefits accompanied by enhanced ghrelin production. Ghrelin receptor (GH secretagogue receptor 1a) agonists administered to aging rodents and humans restore the young adult phenotype; therefore, we tested the hypothesis that the metabolic benefits of CR are mediated by endogenous ghrelin. Three month-old male mice lacking ghrelin (Ghrelin−/−) or ghrelin receptor (Ghsr−/−), and their wild-type (WT) littermates were randomly assigned to 2 groups: ad libitum (AL) fed and CR, where 40% food restriction was introduced gradually to allow Ghrelin−/− and Ghsr−/− mice to metabolically adapt and avoid severe hypoglycemia. Twelve months later, plasma ghrelin, metabolic parameters, ambulatory activity, hypothalamic and liver gene expression, as well as body composition were measured. CR increased plasma ghrelin and des-acyl ghrelin concentrations in WT and Ghsr−/− mice. CR of WT, Ghsr−/−, and Ghrelin−/− mice markedly improved metabolic flexibility, enhanced ambulatory activity, and reduced adiposity. Inactivation of Ghrelin or Ghsr had no effect on AL food intake or food anticipatory behavior. In contrast to the widely held belief that endogenous ghrelin regulates food intake, CR increased expression of hypothalamic Agrp and Npy, with reduced expression of Pomc across genotypes. In the AL context, ablation of ghrelin signaling markedly inhibited liver steatosis, which correlated with reduced Pparγ expression and enhanced Irs2 expression. Although CR and administration of GH secretagogue receptor 1a agonists both benefit the aging phenotype, we conclude the benefits of chronic CR are a consequence of enhanced metabolic flexibility independent of endogenous ghrelin or des-acyl ghrelin signaling.

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