Dietary fat: From foe to friend?

Science ◽  
2018 ◽  
Vol 362 (6416) ◽  
pp. 764-770 ◽  
Author(s):  
David S. Ludwig ◽  
Walter C. Willett ◽  
Jeff S. Volek ◽  
Marian L. Neuhouser
Keyword(s):  
Heart Disease ◽  
Chronic Disease ◽  
Dietary Fat ◽  
Fat Content ◽  
Metabolic Effects ◽  
Dietary Advice ◽  
High Fat ◽  
Ongoing Controversy ◽  
Ketogenic Diets ◽  
Broad Consensus

For decades, dietary advice was based on the premise that high intakes of fat cause obesity, diabetes, heart disease, and possibly cancer. Recently, evidence for the adverse metabolic effects of processed carbohydrate has led to a resurgence in interest in lower-carbohydrate and ketogenic diets with high fat content. However, some argue that the relative quantity of dietary fat and carbohydrate has little relevance to health and that focus should instead be placed on which particular fat or carbohydrate sources are consumed. This review, by nutrition scientists with widely varying perspectives, summarizes existing evidence to identify areas of broad consensus amid ongoing controversy regarding macronutrients and chronic disease.

scholarly journals Regulation of plasma leptin in mice: influence of age, high-fat diet, and fasting

1997 ◽  
Vol 273 (1) ◽  
pp. R113-R120 ◽  
Author(s):  
B. Ahren ◽  
S. Mansson ◽  
R. L. Gingerich ◽  
P. J. Havel
Keyword(s):  
Body Weight ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Age Groups ◽  
Fat Content ◽  
High Fat ◽  
Background Strain ◽  
Plasma Leptin

Mechanisms regulating circulating leptin are incompletely understood. We developed a radioimmunoassay for mouse leptin to examine the influence of age, dietary fat content, and fasting on plasma concentrations of leptin in the background strain for the ob/ob mouse, the C57BL/6J mouse. Plasma leptin increased with age [5.3 +/- 0.6 ng/ml at 2 mo (n = 23) vs. 14.2 +/- 1.6 ng/ml at 11 mo (n = 15), P < 0.001]. Across all age groups (2-11 mo, n = 160), log plasma leptin correlated with body weight (r = 0.68, P < 0.0001), plasma insulin (r = 0.38, P < 0.001), and amount of intra-abdominal fat (r = 0.90, P < 0.001), as revealed by magnetic resonance imaging. Plasma leptin was increased by a high-fat diet (58% fat for 10 mo) and reduced by fasting for 48 h. The reduction of plasma leptin was correlated with the reduction of plasma insulin (r = 0.43, P = 0.012) but not with the initial body weight or the change in body weight. Moreover, the reduction in plasma leptin by fasting was impaired by high-fat diet. Thus plasma leptin in C57BL/6J mice 1) increases with age or a high-fat diet; 2) correlates with body weight, fat content, and plasma insulin; and 3) is reduced during fasting by an action inhibited by high-fat diet and related to changes of plasma insulin.

Impact of graded maternal dietary fat content on offspring susceptibility to high‐fat diet in mice

Obesity ◽  
2021 ◽  
Vol 29 (12) ◽  
pp. 2055-2067
Author(s):  
Yi Huang ◽  
Jazmin Osorio Mendoza ◽  
Min Li ◽  
Zengguang Jin ◽  
Baoguo Li ◽  
...  
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
High Fat

scholarly journals Temporal and dietary fat content–dependent islet adaptation to high-fat feeding–induced glucose intolerance in mice

Metabolism ◽  
2007 ◽  
Vol 56 (1) ◽  
pp. 122-128 ◽  
Author(s):  
Maria Sörhede Winzell ◽  
Caroline Magnusson ◽  
Bo Ahrén
Keyword(s):  
Glucose Intolerance ◽  
Dietary Fat ◽  
Fat Content ◽  
High Fat ◽  
Fat Feeding

scholarly journals Programming With Varying Dietary Fat Content Alters Cardiac Insulin Receptor, Glut4 and FoxO1 Immunoreactivity in Neonatal Rats, Whereas High Fat Programming Alters Cebpa Gene Expression in Neonatal Female Rats

2022 ◽  
Vol 12 ◽  
Author(s):  
Annelene Govindsamy ◽  
Samira Ghoor ◽  
Marlon E. Cerf
Keyword(s):  
Gene Expression ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Female Offspring ◽  
Fat Content ◽  
Neonatal Rats ◽  
Cardiac Physiology ◽  
High Fat

Fetal programming refers to an intrauterine stimulus or insult that shapes growth, development and health outcomes. Dependent on the quality and quantity, dietary fats can be beneficial or detrimental for the growth of the fetus and can alter insulin signaling by regulating the expression of key factors. The effects of varying dietary fat content on the expression profiles of factors in the neonatal female and male rat heart were investigated and analyzed in control (10% fat), 20F (20% fat), 30F (30% fat) and 40F (40% fat which was a high fat diet used to induce high fat programming) neonatal rats. The whole neonatal heart was immunostained for insulin receptor, glucose transporter 4 (Glut4) and forkhead box protein 1 (FoxO1), followed by image analysis. The expression of 84 genes, commonly associated with the insulin signaling pathway, were then examined in 40F female and 40F male offspring. Maintenance on diets, varying in fat content during fetal life, altered the expression of cardiac factors, with changes induced from 20% fat in female neonates, but from 30% fat in male neonates. Further, CCAAT/enhancer-binding protein alpha (Cebpa) was upregulated in 40F female neonates. There was, however, differential expression of several insulin signaling genes in 40F (high fat programmed) offspring, with some tending to significance but most differences were in fold changes (≥1.5 fold). The increased immunoreactivity for insulin receptor, Glut4 and FoxO1 in 20F female and 30F male neonatal rats may reflect a compensatory response to programming to maintain cardiac physiology. Cebpa was upregulated in female offspring maintained on a high fat diet, with fold increases in other insulin signaling genes viz. Aebp1, Cfd (adipsin), Adra1d, Prkcg, Igfbp, Retn (resistin) and Ucp1. In female offspring maintained on a high fat diet, increased Cebpa gene expression (concomitant with fold increases in other insulin signaling genes) may reflect cardiac stress and an adaptative response to cardiac inflammation, stress and/or injury, after high fat programming. Diet and the sex are determinants of cardiac physiology and pathophysiology, reflecting divergent mechanisms that are sex-specific.

scholarly journals Macronutrient balances and obesity: the role of diet and physical activity

1999 ◽  
Vol 2 (3a) ◽  
pp. 341-347 ◽  
Author(s):  
Arne Astrup
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Physical Fitness ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Oxidation ◽  
Fat Content ◽  
High Fat

AbstractObservational cross-sectional and longitudinal studies suggest that a high fat diet and physical inactivity are independent risk factors for weight gain and obesity. Mechanistic and intervention studies support that fat possesses a lower satiating power than carbohydrate and protein, and a diet low in fat therefore decreases energy intake. The effect of dietary fat on energy balance is enhanced in susceptible subjects, particularly in sedentary individuals with a genetic predisposition to obesity who consume a high fat diet.Dietary carbohydrate promotes its own oxidation by an insulin-mediated stimulation of glucose oxidation. In contrast, high fat meals do not increase fat oxidation acutely. A sedentary life-style and low physical fitness cause a low muscular fat oxidation capacity, and the consumption of a high fat diet by these individuals promotes fat storage in a synergistic fashion.Ad libitum low fat diets cause weight loss proportional to pre-treatment body weight in a dose-dependent way, i.e. weight loss is correlated positively to the reduction in dietary fat content. Increased physical activity prevents relapse after weight loss and studies have shown that those who keep up a higher level of physical activity are more successful in maintaining the reduced body weight. In conclusion, important interactions exist between genetic make up, dietary fat and physical fitness, so that a low fitness level and susceptible genes reduce muscular fat oxidation capacity which may decrease the tolerance of dietary fat. Increasing daily physical activity and reducing dietary fat content may be more effective when combined than when separate in preventing weight gain and obesity.

Dietary fat and low fiber in purified diets differently impact the gut-liver axis to promote obesity-linked metabolic impairments

2021 ◽  
Author(s):  
Noëmie Daniel ◽  
Laίs Rossi Perazza ◽  
Thibault V. Varin ◽  
Jocelyn Trottier ◽  
Bruno Marcotte ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Fat ◽  
Fat Content ◽  
Fiber Content ◽  
Gut Health ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Microbial Composition ◽  
The Impact ◽  
Metabolic Impairments

Purified high-fat diets are commonly used to promote obesity and metabolic disturbances in animal models. However, most studies also use unpurified chow (low in fat, high in fiber content) as a "healthy" diet which can impact gut health. Here, we investigated the impact of feeding chow or purified diets varying in fat content on metabolic and intestinal functions in relation with temporal changes in gut microbiota composition. C57BL/6J male mice were fed either chow or purified low-fat (LF) or high-fat (HF) diet for 12 weeks. LF-fed mice displayed similar glucose and insulin homeostasis and bile acid profile than chow-fed mice but did exhibit higher fasting insulinemia and impaired insulin clearance, which was associated with increased weight gain and fat mass. Compared with chow, feeding LF or HF diets increased hepatic steatosis and inflammation, and impaired intestinal integrity. Changes in gut microbiota preceded these effects, with both purified diets inducing rapid and dramatic decrease of bacterial diversity and short chain fatty acid (SCFA) production. Importantly, branched SCFA levels increased only in HF-fed mice suggesting that this response is driven by excessive dietary fat rather than lack of fiber content. LF-fed mucus-associated microbial composition was also closer to that of chow-fed mice than that of HF-fed mice, suggesting the impact of fat content on this specific microbial community. We have identified distinct and overlapping gut microbiome and metabolic impairments caused by low fiber or high-fat contents in HF-fed animals, revealing their selective mechanisms underpinning the gastrointestinal and metabolic impacts in obesity

Leptin action is modified by an interaction between dietary fat content and ambient temperature

2004 ◽  
Vol 287 (5) ◽  
pp. R1250-R1255 ◽  
Author(s):  
Andrea L. Haltiner ◽  
Tiffany D. Mitchell ◽  
Ruth B. S. Harris
Keyword(s):  
Energy Intake ◽  
Body Fat ◽  
Dietary Fat ◽  
Leptin Receptor ◽  
Environmental Temperature ◽  
Short Form ◽  
Uncoupling Protein ◽  
Fat Content ◽  
High Fat ◽  
Leptin Receptors

Mice adapted to a high-fat diet are reported to be leptin resistant; however, we previously reported that mice fed a high-fat (HF) diet and housed at 23°C remained sensitive to peripheral leptin and specifically lost body fat. This study tested whether leptin action was impaired by a combination of elevated environmental temperature and a HF diet. Male C57BL/6 mice were adapted to low-fat (LF) or HF diet from 10 days of age and were housed at 27°C from 28 days of age. From 35 days of age, baseline food intake and body weight were recorded for 1 wk and then mice on each diet were infused with 10 μg leptin/day or PBS from an intraperitoneal miniosmotic pump for 13 days. HF-fed mice had a higher energy intake than LF-fed mice and were heavier but not fatter. Serum leptin was lower in PBS-infused HF- than LF-fed mice. Leptin significantly inhibited energy intake of both LF-fed and HF-fed mice, and this was associated with a significant increase in hypothalamic long-form leptin receptors with no change in short-form leptin receptor or brown fat uncoupling protein-1 mRNA expression. Leptin significantly inhibited weight gain in both LF- and HF-fed mice but reduced the percentage of body fat mass only in LF-fed mice. The percentage of lean and fat tissue in HF-fed mice did not change, implying that overall growth had been inhibited. These results suggest that dietary fat modifies the mechanisms responsible for leptin-induced changes in body fat content and that those in HF-fed mice are sensitive to environmental temperature.

scholarly journals Dietary fat and corticosterone levels are contributing factors to meal anticipation

2016 ◽  
Vol 310 (8) ◽  
pp. R711-R723 ◽  
Author(s):  
Sara Namvar ◽  
Amy Gyte ◽  
Mark Denn ◽  
Brendan Leighton ◽  
Hugh D. Piggins
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Content ◽  
High Fat ◽  
Contributing Factors ◽  
Low Fat ◽  
Restricted Access ◽  
Fos Expression ◽  
Fat Feeding

Daily restricted access to food leads to the development of food anticipatory activity and metabolism, which depends upon an as yet unidentified food-entrainable oscillator(s). A premeal anticipatory peak in circulating hormones, including corticosterone is also elicited by daily restricted feeding. High-fat feeding is associated with elevated levels of corticosterone with disrupted circadian rhythms and a failure to develop robust meal anticipation. It is not clear whether the disrupted corticosterone rhythm, resulting from high-fat feeding contributes to attenuated meal anticipation in high-fat fed rats. Our aim was to better characterize meal anticipation in rats fed a low- or high-fat diet, and to better understand the role of corticosterone in this process. To this end, we utilized behavioral observations, hypothalamic c-Fos expression, and indirect calorimetry to assess meal entrainment. We also used the glucocorticoid receptor antagonist, RU486, to dissect out the role of corticosterone in meal anticipation in rats given daily access to a meal with different fat content. Restricted access to a low-fat diet led to robust meal anticipation, as well as entrainment of hypothalamic c-Fos expression, metabolism, and circulating corticosterone. These measures were significantly attenuated in response to a high-fat diet, and animals on this diet exhibited a postanticipatory rise in corticosterone. Interestingly, antagonism of glucocorticoid activity using RU486 attenuated meal anticipation in low-fat fed rats, but promoted meal anticipation in high-fat-fed rats. These findings suggest an important role for corticosterone in the regulation of meal anticipation in a manner dependent upon dietary fat content.

Failure to increase lipid oxidation in response to increasing dietary fat content in formerly obese women

1994 ◽  
Vol 266 (4) ◽  
pp. E592-E599 ◽  
Author(s):  
A. Astrup ◽  
B. Buemann ◽  
N. J. Christensen ◽  
S. Toubro
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Matched Control ◽  
Fat Content ◽  
Carbohydrate Oxidation ◽  
Control Group ◽  
Obese Women ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

The effect of an increase in dietary fat content on fat and carbohydrate balances and energy expenditure (EE) was studied in nine formerly obese women with genetic predisposition to obesity (postobese) and a closely matched control group. Isocaloric low- (20% fat energy) and high-fat diets (50%) were consumed for 3 days preceding and during a 24-h respiratory chamber stay, whereas a medium-fat diet (30%) was consumed only on the day of measurement. After adjustment for 24-h energy intake to equal 24-h EE, 24-h fat balance was increased when the dietary fat content increased (P < 0.0002). No differences in macronutrient balances were found on the low-fat and medium-fat diets, but on the high-fat diet the postobese women failed to increase ratio of fat to carbohydrate oxidation appropriately (0.59 g/g, 95% confidence interval 0.47-0.67 vs. controls 1.02 g/g, 0.88–1.12; P = 0.002). This caused a positive adjusted fat balance (+11.0 g/day, 2.3–19.6 vs. controls -8.9 g/day, -17.5 to -0.2; P < 0.001) and a negative carbohydrate balance (-41.8 g/day, -69.5 to -14.0 vs. controls +23.2 g/day, -4.6 to +50.9; P < 0.001). Decreasing the dietary fat content increased 24-h EE in the postobese women (P = 0.02), whereas it was unaffected in the control group. Independent of energy balance, an increase in dietary fat content to 50% fat energy results in preferential fat storage, impaired suppression of carbohydrate oxidation, and reduction of 24-h EE in postobese women.

A high-fat, ketogenic diet induces a unique metabolic state in mice

2007 ◽  
Vol 292 (6) ◽  
pp. E1724-E1739 ◽  
Author(s):  
Adam R. Kennedy ◽  
Pavlos Pissios ◽  
Hasan Otu ◽  
Bingzhong Xue ◽  
Kenji Asakura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Energy Expenditure ◽  
Ketogenic Diet ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
High Fat ◽  
Metabolic State ◽  
Ketogenic Diets ◽  
Low Carbohydrate

Ketogenic diets have been used as an approach to weight loss on the basis of the theoretical advantage of a low-carbohydrate, high-fat diet. To evaluate the physiological and metabolic effects of such diets on weight we studied mice consuming a very-low-carbohydrate, ketogenic diet (KD). This diet had profound effects on energy balance and gene expression. C57BL/6 mice animals were fed one of four diets: KD; a commonly used obesogenic high-fat, high-sucrose diet (HF); 66% caloric restriction (CR); and control chow (C). Mice on KD ate the same calories as mice on C and HF, but weight dropped and stabilized at 85% initial weight, similar to CR. This was consistent with increased energy expenditure seen in animals fed KD vs. those on C and CR. Microarray analysis of liver showed a unique pattern of gene expression in KD, with increased expression of genes in fatty acid oxidation pathways and reduction in lipid synthesis pathways. Animals made obese on HF and transitioned to KD lost all excess body weight, improved glucose tolerance, and increased energy expenditure. Analysis of key genes showed similar changes as those seen in lean animals placed directly on KD. Additionally, AMP kinase activity was increased, with a corresponding decrease in ACC activity. These data indicate that KD induces a unique metabolic state congruous with weight loss.

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