Hypercaloric diets with increased meal frequency, but not meal size, increase intrahepatic triglycerides: A randomized controlled trial

Abstract

American children consume up to 27% of calories from high-fat and high-sugar snacks. Both sugar and fat consumption have been implicated as a cause of hepatic steatosis and obesity but the effect of meal pattern is largely understudied. We hypothesized that a high meal frequency, compared to consuming large meals, is detrimental in the accumulation of intrahepatic and abdominal fat. To test this hypothesis, we randomized 36 lean, healthy men to a 40% hypercaloric diet for 6 weeks or a eucaloric control diet and measured intrahepatic triglyceride content (IHTG) using proton magnetic resonance spectroscopy (1H-MRS), abdominal fat using magnetic resonance imaging (MRI), and insulin sensitivity using a hyperinsulinemic euglycemic clamp with a glucose isotope tracer before and after the diet intervention. The caloric surplus consisted of fat and sugar (high-fat-high-sugar; HFHS) or sugar only (high-sugar; HS) and was consumed together with, or between, the three main meals, thereby increasing meal size or meal frequency. All hypercaloric diets similarly increased body mass index (BMI). Increasing meal frequency significantly increased IHTG (HFHS mean relative increase of 45%; P = 0.016 and HS mean relative increase of 110%; P = 0.047), whereas increasing meal size did not (2-way analysis of variance [ANOVA] size versus frequency P = 0.03). Abdominal fat increased in the HFHS-frequency group (+63.3 ± 42.8 mL; P = 0.004) and tended to increase in the HS-frequency group (+46.5 ± 50.7 mL; P = 0.08). Hepatic insulin sensitivity tended to decrease in the HFHS-frequency group while peripheral insulin sensitivity was not affected. Conclusion: A hypercaloric diet with high meal frequency increased IHTG and abdominal fat independent of caloric content and body weight gain, whereas increasing meal size did not. This study suggests that snacking, a common feature in the Western diet, independently contributes to hepatic steatosis and obesity. (Trial registration: http://www.forestplots.net; nr.NCT01297738.) (Hepatology 2014;60:545–553)

Potential link between excess added sugar intake and ectopic fat: a systematic review of randomized controlled trials

“…Effect of increased or reduced added sugar intake on fat depots Table 2 13,31-36 summarizes the results from 7 randomized controlled intervention trials: 6 in adults 13,[31][32][33][34][35] and 1 in children. 36 The 6 studies in adults were designed to compare sugar intake as part of a hypercaloric diet with intake of a eucaloric control diet that Full text articles excluded because 1) not relevant to study objective; 2) using same study sample (in this case, only one study was included in the present review); 3) single arm trial; 4) observational studies (no prospective): n=27 contained no excess sugars.…”

“…As such, these studies were confounded by energy intake, and therefore one cannot separate out the effects of energy and sugar. In the studies of Koopman et al 31 and Maersk et al, 13 surplus energy was provided from the daily consumption of 1 L of sucrose-sweetened cola. In 4 trials, fructose or glucose or both were added to a weight-maintaining diet to create a hypercaloric diet that was then compared with a weight-maintaining diet alone.…”

“…In adults, liver fat was measured in 6 studies, 13,[31][32][33][34][35] VAT in 1 study, 13 and muscle fat in 2 studies. 33,35 Metaanalyses were performed to examine the pooled effect of high-sugar hypercaloric diets on liver and muscle fat deposition compared with the effect of a eucaloric control diet.…”

Metabolic impacts of altering meal frequency and timing – Does when we eat matter?

“…Furthermore, prescribing for increased eating opportunities must be carefully considered in today's obesogenic environment, since this may inadvertently result in over-consumption and weight gain [22e25]. This is especially important in light of recent evidence that shows that overconsumption of energy-dense foods with increased frequency results in poorer metabolic health [26].…”

The Effects of Different High-Protein Low-Carbohydrates Proprietary Foods on Blood Sugar in Healthy Subjects

“…Postprandial hyperglycemia and compensatory hypoglycemia are factors linked to the development of diabetes and cardiovascular diseases 33 . Furthermore, the consumption of high-sugar snacks seems to be the main cause for the increase in intrahepatic triglyceride content (IHTG) 34 . Finally, the usual rapid and high glycemic peak caused by ultra-processed products, together with their lack in fiber, proteins and water, triggers an excessive consumption 19,35 .…”