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Proton magnetic resonance spectroscopy reveals increased hepatic lipid content after a single high-fat meal with no additional modulation by added protein

Background: Fat accumulation in nonadipose tissue is linked to insulin resistance and metabolic diseases. Earlier studies have shown that hepatic lipid accumulation can occur after 4 d of a high-fat diet in humans, and this fat accumulation can be blunted by the ingestion of additional proteins.

Objectives: In this study, we explored whether a single high-fat meal increased the lipid content in liver and skeletal muscle as measured by using in vivo proton magnetic resonance spectroscopy (1H-MRS) and whether the addition of protein can modulate the postprandial ectopic lipid storage.

Design: Intrahepatic lipid (IHL) and intramyocellular lipid (IMCL) concentrations were determined by using 1H-MRS before and 3 and 5 h after a high-fat with added protein meal (61.% of energy from fat) or a high-fat without added protein meal (mean ± SEM: 51.1 ± 7.9 g of protein; 191.9 ± 9.9 kcal added) in a randomized crossover study. IHL and IMCL concentrations were converted to absolute concentrations (g/kg wet weight) by using water as an internal reference.

Results: Nine lean, healthy subjects [6 men and 3 women; mean (±SD) age: 22.7 ± 3.0 y; mean body mass index (in kg/m2): 21.8 ± 1.8] were included in this study. IHL concentrations were increased 20% (P < 0.01) at 3 h after the meal and did not further increase after 5 h. In contrast, IMCL concentrations were not altered during the postprandial period (P = 0.74). The addition of protein to a single high-fat meal did not change the postprandial accumulation of fat in the liver (P = 0.93) or skeletal muscle (P = 0.84).

Conclusions: In this study, we showed that a single energy-dense, high-fat meal induced the net lipid accumulation in the liver, which was detected by using in vivo1H-MRS. This noninvasive approach might bring new opportunities to study postprandial hepatic lipid dynamics. The addition of protein did not change the ectopic lipid retention after a single high-fat meal. 


Alex’s Notes: Last week we found out that on a weight-stable diet, a high-fat and high-saturated fat diet does not increase liver fat, while a low-fat diet reduces liver fat. But what happens when we eat a high-fat meal? That is exactly what the current study was determined to find out. Moreover, given that it was previously shown that adding protein to a high-fat meal blunts liver fat accumulation, this study sought to verify these effects utilizing more advanced and accurate investigative methods (namely, the use of proton magnetic resonance spectroscopy (H-MRS).

Nine healthy, young, lean men (n=6) and women (n=3) participated in the study. The average age was about 23-years, and the average body fat percentage was 11% for men and 23% for women, determined by hydrostatic weighing. In a randomized crossover design, the subjects consumed an energy-dense high-fat meal (HF) or the same meal with added protein (HFP) after a 10.5 hour fast. Two days before test days, subjects were asked to refrain from strenuous physical activity and alcohol consumption, and the evenings before both test days, they consumed a provided standardized meal (505 kcal; 33% fat, 53%, and 14% protein). The washout period between trials was one week.

The HF meal consisted of sausage rolls containing 61.5% energy from fat, 31.6% energy from carbohydrates, and 6.9% energy from proteins that were dosed to equal 50% of the subjects’ daily recommended caloric intakes, as determined by the Cunningham formula with an activity factor of 1.3. For the HFP meal, a concentrated milk protein powder was dissolved in water and provided to subjects to drink with their HF meal. The amount of protein added was calculated to ensure that the total energy content from the protein in the meal equaled 20%.

Unfortunately, the researchers don’t provide a more descriptive breakdown of the meals, so it is impossible to tell how much of the fat was saturated and unsaturated. Moreover, these were not just high fat meals, but also high carbohydrate meals, and the composition of the form of carbohydrate isn’t provided. That said, the information that is provided about the meals appears in the table below.





Total Energy Content

1169 kcal

1361 kcal

192 kcal













Hepatic fat content (IHL) significantly increased by 19% from baseline to three hours in the HF feeding and by 27% in the HFP feeding. Despite the small difference in magnitude, it was not statistically significant between the trials, and there was no significant difference between IHL from 3 to 5 hours, but the 5 hour concentrations were sill significantly elevated compared to baseline values. Conversely, intra-muscular fat content (IMCL) was not significantly different following the meals or between meal types. Sex had no influence on anything.

As would be expected by the carbohydrate bolus in the meals, insulin levels rose and fell post-prandial, with the main effect of the meal approaching significance (p=0.07) and the overall insulin response being greater in the HFP group. These same observations were made for triglycerides concentrations with the HFP meal resulting in significantly greater post-prandial area-under-the-curve, but there was no difference between groups in the glucose and free fatty acid responses to the meals.


There was a rather strong and significant positive association between insulin (r=0.74) and IHL concentrations at 3 hours, as well as between IHL concentrations and triglycerides (r=0.83). This held true for the 5 hour mark also. These correlations were not present in the HF meal trials. So how can there be more insulin and triglycerides but equivalent liver fat? The authors speculate that this could be the result of increased de novo lipogenesis (from insulin) that contributes to increased VLDL secretion (more triglycerides). Unfortunately, one limitation of the H-MRS method is the inability to differentiate between dietary and endogenous fats.

Food for thought

This got me thinking. Many people backload their carbohydrates and eat most their fat in the morning meals. Since protein doesn’t appear to play a huge role, let’s ignore it for a moment. If liver fat remains elevated for five hours after a fatty meal, and liver fat is central to insulin resistance, would it be so off-base to speculate that the carbohydrate meal later in the day may run into an acute insulin resistance situation brought about by the morning feeding? Perhaps after five hours the levels normalize, but given that they were hardly changed from the 3-hour mark, they may stay elevated for some time. We don’t know. We also don’t know how great an impact this slight elevation would have on insulin signaling, or even if this hepatic accumulation of lipids would occur in the absence of carbohydrates. The meals contained an astonishing 92g of carbohydrates, and overall the meals made up 50% your daily calories.

So, food for thought. Definitely interesting and I will be keeping an eye out for future studies looking at the impact of both acute and chronic fat intake on various health markers.


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