Increasing Protein Intake Modulates Lipid Metabolism in Healthy Young Men and Women Consuming a High-Fat Hypercaloric Diet

Abstract

The objective of this study was to evaluate the effect of increasing protein intake, at the expense of carbohydrates, on intrahepatic lipids (IHLs), circulating triglycerides (TGs), and body composition in healthy humans consuming a high-fat, hypercaloric diet. A crossover randomized trial with a parallel control group was performed. After a 2-wk run-in period, participants were assigned to either the control diet [n = 10; 27.8 energy percent (en%) fat, 16.9 en% protein, 55.3 en% carbohydrates] for 4 wk or a high-fat, hypercaloric diet (n = 17; >2 MJ/d) crossover trial with 2 periods of 2 wk, with either high-protein (HP) (37.7 en% fat, 25.7 en% protein, 36.6 en% carbohydrates) or normal-protein (NP) (39.4 en% fat, 15.4 en% protein, 45.2 en% carbohydrates) content. Measurements were performed after 2 wk of run-in (baseline), 2 wk of intervention (period 1), and 4 wk of intervention (period 2). A trend toward lower IHL and plasma TG concentrations during the HP condition compared with the NP condition was observed (IHL: 0.35 ± 0.04% vs. 0.51 ± 0.08%, P = 0.08; TG: 0.65 ± 0.03 vs. 0.77 ± 0.05 mmol/L, P = 0.07, for HP and NP, respectively). Fat mass was significantly lower (10.6 ± 1.72 vs. 10.9 ± 1.73 kg; P = 0.02) with the HP diet than with the NP diet, whereas fat-free mass was higher (55.7 ± 2.79 vs. 55.2 ± 2.80 kg; P = 0.003). This study indicated that an HP, high-fat, hypercaloric diet affects lipid metabolism. It tends to lower the IHL and circulating TG concentrations and significantly lowers fat mass and increases fat-free mass compared with an NP, high-fat, hypercaloric diet. This trail was registered at www.clinicaltrials.gov as NCT01354626.

Short term elevation in dietary protein intake does not worsen insulin resistance or lipids in older adults with metabolic syndrome: a randomized-controlled trial

“…Meta-analysis of high protein/weight loss studies has confirmed their preferential efficacy on the reduction of triglycerides in particular [40]. In the case of a hypercaloric diet, increased protein intake is linked to a trend (i.e., p = 0.07) towards reduced triglycerides [7]. In our study under conditions of weight balance and isocaloric dietary intake, we found no improvements in any of the lipid panels (Table 4).…”

“…Given that skeletal muscle is the largest organ and responsible for the majority of post-prandial glucose disposal [5], an increase in protein intake may promote the preservation of skeletal muscle and lead to improvements in insulin sensitivity [6]. Studies have also shown that increased protein intake may have favorable effects on circulating triglyceride concentrations [7]. Indeed, elevations in protein intake have been linked to many improvements in what many consider the hallmarks of metabolic syndrome (i.e., hypertension, atherosclerosis, hyperlipidemia) [8].…”

Hepatic fatty acid biosynthesis is more responsive to protein than carbohydrate in rainbow trout during acute stimulations

“…(15) and in vivo observations reporting that high-proteinlow-carbohydrate diets stimulated lipogenic gene expression (FAS and SREBP1) and enzyme activity (FAS, G6PDH, and ME) compared with low-protein-high-carbohydrate diets in rainbow trout and blackspot seabream, respectively (23,75). However, these results are different from the demonstrations in rodents, chickens, or humans reporting that high-protein (HP) diets induce downregulations of fatty acid biosynthesis in liver at both gene expression and enzymatic levels (1,2,7,56,64,67,87,90). Data from mice have shown that an increased flux of AAs reaching the hepatoportal area in HP diet conditions promotes AA catabolism and acetyl-CoA synthesis; however, it was suggested that the synthesized acetyl-CoA is either channeled into the TCA cycle or used for ␤-hydroxybutyrate production, but not converted to fatty acids through unknown reasons (64,72,92).…”

“…However, these results are different from the demonstrations in rodents, chickens, or humans reporting that high-protein (HP) diets induce downregulations of fatty acid biosynthesis in liver at both gene expression and enzymatic levels (1,2,7,56,64,67,87,90). Data from mice have shown that an increased flux of AAs reaching the hepatoportal area in HP diet conditions promotes AA catabolism and acetyl-CoA synthesis; however, it was suggested that the synthesized acetyl-CoA is either channeled into the TCA cycle or used for ␤-hydroxybutyrate production, but not converted to fatty acids through unknown reasons (64,72,92). Therefore, DNL rates might be lower or even absent after an HP diet (72).…”

“…Finally, glucose stimulates the release of insulin from the pancreas, thereby activating insulin/Akt signaling pathway (40,69), which stimulates hepatic lipogenesis via the transcription factor sterol regulatory element binding protein-1c (SREBP-1c) (32). Regarding dietary protein, rodent data showed that the metabolic adaptation to a high-protein diet included a downregulation of lipogenesis at both gene expression and enzymatic levels (64). Notably, the activity of lipogenic pathway also depends on the availability of cofactors, such as NADPH, produced by the pentose phosphate pathway (27), and DNL may serve as a key regulator in tandem with elongation and desaturation (10,13,36).…”