scholarly journals High dietary protein decreases fat deposition induced by high-fat and high-sucrose diet in rats

2015 ◽  
Vol 114 (8) ◽  
pp. 1132-1142 ◽  
Author(s):  
Catherine Chaumontet ◽  
Patrick C. Even ◽  
Jessica Schwarz ◽  
Angélique Simonin-Foucault ◽  
Julien Piedcoq ◽  
...  

AbstractHigh-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver.

2011 ◽  
Vol 70 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Kevin D. Tipton

Athletes and exercisers have utilised high-protein diets for centuries. The objective of this review is to examine the evidence for the efficacy and potential dangers of high-protein diets. One important factor to consider is the definition of a ‘high-protein diet’. There are several ways to consider protein content of a diet. The composition of the diet can be determined as the absolute amount of the protein (or other nutrient of interest), the % of total energy (calories) as protein and the amount of protein ingested per kg of body weight. Many athletes consume very high amounts of protein. High-protein diets most often are associated with muscle hypertrophy and strength, but now also are advocated for weight loss and recovery from intense exercise or injuries. Prolonged intake of a large amount of protein has been associated with potential dangers, such as bone mineral loss and kidney damage. In otherwise healthy individuals, there is little evidence that high protein intake is dangerous. However, kidney damage may be an issue for individuals with already existing kidney dysfunction. Increased protein intake necessarily means that overall energy intake must increase or consumption of either carbohydrate or fat must decrease. In conclusion, high protein intake may be appropriate for some athletes, but there are potential negative consequences that must be carefully considered before adopting such a diet. In particular, care must be taken to ensure that there is sufficient intake of other nutrients to support the training load.


1992 ◽  
Vol 67 (2) ◽  
pp. 223-233 ◽  
Author(s):  
J. G. H. Sterck ◽  
J. Ritskes-Hoitinga ◽  
A. C. Beynen

Increased intakes of protein have been shown to reduce kidney calcification (nephrocalcinosis) in female rats. Two questions were addressed in the present study. First, can protein-induced inhibition of nephrocalcinosis be demonstrated when the diets used are balanced for calcium, magnesium and phosphorus in the added protein? Second, can the protein effect be explained by the frequently observed magnesiuria after giving high-protein diets? Nephrocalcinosis was induced in female rats by giving purified diets containing 151 g casein/kg and either an increased concentration of P (6 v. 2 g/kg) or a decreased concentration of Mg (0·1 v. 0·4 g/kg). To these diets 151 g ovalbumin/kg was added at the expense of glucose, and the diets were balanced for Ca, Mg and P in ovalbumin. The diets were given for 29 d. In rats fed on the diet containing 151 g protein/kg, an increased intake of P or a decreased intake of Mg caused nephrocalcinosis as measured chemically by analysis of kidney Ca as well as histologically by scoring kidney sections stained according to Von Kossa's method. The addition of ovalbumin to the diet prevented the induction of nephrocalcinosis. High P intake and low Mg intake with the low-protein diets induced enhanced loss of albumin in urine, suggesting that nephrocalcinosis caused kidney damage. Increased protein intake with a non-calcinogenic diet also caused increased albumin excretion in urine. Irrespective of the composition of the background diet, increased protein intake caused increased urinary excretion of Mg. When all dietary groups were considered, differences in nephrocalcinosis and urinary Mg output were not proportionally related.Nephrocalcinosis: Phosphorus: Magnesium: Protein: Rat


2020 ◽  
Vol 31 (8) ◽  
pp. 1667-1679 ◽  
Author(s):  
Gang-Jee Ko ◽  
Connie M. Rhee ◽  
Kamyar Kalantar-Zadeh ◽  
Shivam Joshi

Although high-protein diets continue to be popular for weight loss and type 2 diabetes, evidence suggests that worsening renal function may occur in individuals with—and perhaps without—impaired kidney function. High dietary protein intake can cause intraglomerular hypertension, which may result in kidney hyperfiltration, glomerular injury, and proteinuria. It is possible that long-term high protein intake may lead to de novo CKD. The quality of dietary protein may also play a role in kidney health. Compared with protein from plant sources, animal protein has been associated with an increased risk of ESKD in several observational studies, including the Singapore Chinese Health Study. Potential mediators of kidney damage from animal protein include dietary acid load, phosphate content, gut microbiome dysbiosis, and resultant inflammation. In light of such findings, adopting current dietary approaches that include a high proportion of protein for weight reduction or glycemic control should be considered with care in those at high risk for kidney disease. Given the possibility of residual confounding within some observational studies and the conflicting evidence from previous trials, long-term studies including those with large sample sizes are warranted to better ascertain the effects of high protein intake on kidney health.


Diabetologia ◽  
2004 ◽  
Vol 48 (1) ◽  
pp. 8-16 ◽  
Author(s):  
K. A. McAuley ◽  
C. M. Hopkins ◽  
K. J. Smith ◽  
R. T. McLay ◽  
S. M. Williams ◽  
...  

1967 ◽  
Vol 105 (2) ◽  
pp. 771-777 ◽  
Author(s):  
D G Walker ◽  
Susan W. Eaton

1. Feeding a high-glucose diet to weanling rats showed that high hepatic glucokinase activities could be induced at 18 days of age, i.e. 2 days after development of the enzyme begins. 2. The normal development of glucokinase activity can be retarded by weaning rats on to carbohydrate-free, high-fat and high-protein diets. 3. Precocious development of the enzyme before 16 days of age cannot be induced by oral glucose administration. 4. It is concluded that the ability to synthesize glucokinase develops very rapidly and that the nature of the diet determines the normal developmental pattern.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Laure Chevalier ◽  
Cécile Bos ◽  
Dalila Azzout‐Marniche ◽  
Gilles Fromentin ◽  
Daniel Tomé ◽  
...  

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