Low-protein High-carbohydrate Diet Research Articles

Dietary protein restriction diminishes sucrose reward and reduces sucrose-evoked mesolimbic dopamine signaling in mice

A growing literature suggests manipulating dietary protein status decreases sweet consumption in rodents and in humans. Underlying neurocircuit mechanisms have not yet been determined, but previous work points towards hedonic rather than homeostatic pathways. Here we hypothesized that a history of protein restriction reduces sucrose seeking by altering mesolimbic dopamine signaling in mice. We tested this hypothesis using established behavioral tests of palatability and conditioned reward, including the palatability contrast and conditioned place preference (CPP) tests. We used modern optical sensors for measuring real-time nucleus accumbens (NAc) dopamine dynamics during voluntary sucrose consumption, via fiber photometry, in male C57/Bl6J mice maintained on low-protein high-carbohydrate (LPHC) or control (CON) diet for ∼5 weeks. Our results showed that a history of protein restriction decreased the consumption of a sucrose ‘dessert’ in sated mice by ∼50% compared to controls [T-test, p < 0.05]. The dopamine release in NAc during sucrose consumption was reduced, also by ∼50%, in LPHC-fed mice compared to CON [T-test, p < 0.01]. Furthermore, LPHC-feeding blocked the sucrose-conditioned place preference we observed in CON-fed mice [paired T-test, p < 0.05], indicating reduced sucrose reward. This was accompanied by a 33% decrease in neuronal activation of the NAc core, as measured by c-Fos immunolabeling from brains collected directly after the CPP test [T-test, p < 0.05]. Together, these findings advance our mechanistic understanding of how dietary protein restriction decreases the consumption of sweets—by inhibiting the incentive salience of a sucrose reward, together with reduced sucrose-evoked dopamine release in NAc.

Larval diet impacts black soldier fly (Diptera: Stratiomyidae) thermal tolerance and preference.

Thermal tolerance and preference are key parameters impacting agricultural production systems. In this study, the impact of larval diet on black soldier fly thermal tolerance and preference across life-stages and sexes was examined. Larvae were fed either a low-protein high-carbohydrate synthetic diet (i.e., P7C35), a high-protein low-carbohydrate synthetic diet (i.e., P35C7), or the Gainesville diet (i.e., C) as a control and reference. Our results demonstrate that the impacts of larval diet on black soldier fly thermal tolerance and preference could be stage and sex specific. The mean heat knockdown temperatures (HKT) ranged between 46.6 and 47.9 °C. Synthetic diets resulted in greater HKT and the difference decreased form larvae (e.g., ∼1 °C) to adults (e.g., ∼0.2 °C). The mean chill-coma recovery time (CCRT) ranged between 8.3 and 21.6 min. Not much differences were detected between diets, but CCRT became longer from larvae to adults. The mean thermal preference ranged between 13.6 and 29.5 °C. Larvae fed synthetic diets preferred much lower temperatures than the control diet. A bimodal distribution was observed for adults regardless of sex. Differences on body mass, lipid, and protein contents were detected among diets; however, more research should be done before any conclusions can be linked to their thermal traits. These findings highlight the importance of considering the ingredients and nutritional makeup of larval diets when optimizing temperature management protocols for mass production of black soldier flies. Conversely, specific diets can be developed to promote survival under extreme rearing temperatures.

Dietary protein restriction diminishes sucrose reward and reduces sucrose-evoked mesolimbic dopamine signaling.

A growing literature suggests manipulating dietary protein status decreases sweet consumption in rodents and in humans. Underlying neurocircuit mechanisms have not yet been determined, but previous work points towards hedonic rather than homeostatic pathways. Here we hypothesized that a history of protein restriction reduces sucrose seeking by altering mesolimbic dopamine signaling. We tested this hypothesis using established behavioral tests of palatability and motivation, including the 'palatability contrast' and conditioned place preference (CPP) tests. We used modern optical sensors for measuring real-time nucleus accumbens (NAc) dopamine dynamics during sucrose consumption, via fiber photometry, in male C57/Bl6J mice maintained on low-protein high-carbohydrate (LPHC) or control (CON) diet for ∼5 weeks. A history of protein restriction decreased the consumption of a sucrose 'dessert' in sated mice by ∼50% compared to controls [T-test, p< 0.05]. The dopamine release in NAc during sucrose consumption was reduced, also by ∼50%, in LPHC-fed mice compared to CON [T-test, p< 0.01]. Furthermore, LPHC-feeding blocked the sucrose-conditioned place preference we observed in CON-fed mice [paired T-test, p< 0.05], indicating reduced motivation. This was accompanied by a 33% decrease in neuronal activation of the NAc core, as measured by c-Fos immunolabeling from brains collected directly after the CPP test. Despite ongoing efforts to promote healthier dietary habits, adherence to recommendations aimed at reducing the intake of added sugars and processed sweets remains challenging. This study highlights chronic dietary protein restriction as a nutritional intervention that suppresses the motivation for sucrose intake, via blunted sucrose-evoke dopamine release in NAc.

High protein-low carbohydrate diet can improve hypoxia tolerance of triploid rainbow trout (Oncorhynchus mykiss): Effects on physiological and metabolic responses to acute hypoxia

Triploid rainbow trout is a hypoxia-sensitive fish species, and is susceptible to death in summer with high water temperature induced acute hypoxia. The study was conducted to evaluate the effect of high protein diet and high carbohydrate diet on hypoxic tolerance of triploid rainbow trout. Two isolipidic and isoenergetic diets with low protein-high carbohydrate level (LPHC) and high protein-low carbohydrate level (HPLC) were specifically formulated. After the feeding trial with 80 days, two group fish were treated with acute hypoxic challenge. Plasma biochemical parameters, hepatic anti-stress, antioxidant and immune related genes expression, and hepatic glucose, lipid, protein and amino acid metabolism related genes expression were then analyzed. The results showed that compared with HPLC diet, LPHC diet could result in excessive plasma levels of alanine aminotransferase (ALT; 36.3 VS 14.0 U/L), aspartate aminotransferase (AST; 978 VS 366 U/L), alkaline phosphatase (ALP; 374 VS 204 U/L), creatine phosphokinase (CPK; 7538 VS 4937 U/L) and lactate dehydrogenase (LDH; 940 VS 451 U/L). In addition, HPLC diet could remodel metabolism of glucose, lipid and protein based on the mRNA expression levels of the genes regulating glycometabolism, lipometabolism, and protein and amino acids metabolism. HPLC diet also enhanced the mRNA expression levels of the genes regulating anti-stress (HSP70, HIF-1a and HIF-2a), antioxidant (Nrf2, SOD, CAT, GPx and HO-1) and immune (IFN-γ, IL-1β, TNF-α and IL-8). In total, LPHC diet could aggravate hypoxic stress of triploid rainbow trout, while HPLC diet could improve fish hypoxic tolerance.

Hepatocyte ballooning and steatosis in early and late gestation without liver malfunction: Effects of low protein/high carbohydrate diet.

Pregnancy is a challenging metabolic and physiological condition. The aim of this study was to include a second demanding situation as a low protein/high carbohydrate diet (LPHCD) to characterize the histological and functional responses of the maternal liver. It is unknown how the maternal liver responds during early and late pregnancy to LPHCD intake. We explored early pregnancy (3 and 8 gestational age, G) and late pregnancy (15 and 20 G). The results indicated that pregnant rats under control diet showed an evident presence of ballooned hepatocytes, lipid vesicles and edema at late pregnancy (15G); in contrast, pregnant rats under LPHCD showed similar pattern of histological modification but at early pregnancy (3G). Unexpectedly, the serum biomarkers didn't display functional alterations in either group, despite of the evident histological changes no liver malfunction was detected. We conclude that pregnant rats fed with control diet and experimental LPHCD, are subjected to metabolic and physiological conditions that impact the histopathological condition of the maternal liver. Control diet promoted the histological modifications during late pregnancy whereas LPCHCD advanced the onset of these changes. Further experiments are needed to explore the biochemical mechanisms that underlie these histological modifications. Our results are also an example of the resilience associated with the pregnancy: since no functional hepatic alterations accompanied the histopathological changes, another conclusion is that no evident pathological condition was detected in this nutritional protocol.

The futile creatine cycle and the synthesis of fatty acids in inguinal white adipose tissue from growing rats, submitted to a hypoprotein-hyperglycidic diet for 15 days.

The low-protein, high-carbohydrate (LPHC) diet administered to growing rats soon after weaning, for 15 days, promoted an increase in energy expenditure by uncoupling protein 1 (UCP1) in interscapular brown adipose tissue, and also due to the occurrence of the browning process in the perirenal white adipose tissue (periWAT). However, we believe that inguinal white adipose tissue (ingWAT) may also contribute to energy expenditure through other mechanisms. Therefore, the aim of this work is to investigate the presence of the futile creatine cycle, and the origin of lipids in ingWAT, since that tissue showed an increase in the lipids content in rats submitted to the LPHC diet for 15 days. We observed increases in creatine kinase and alkaline phosphatase activity in ingWAT, of the LPHC animals. The mitochondrial Nicotinamide adenine dinucleotide reduced/nicotinamide adenine dinucleotide oxidized ratio is lower in ingWAT of LPHC animals. In the LPHC animals treated with β-guanidinopropionic acid, the extracellular uptake of creatine in ingWAT was lower, as was the rectal temperature. Regarding lipid metabolism, we observed that in ingWAT, lipolysis in vitro when stimulated with noradrenaline is lower, and there were no changes in baseline levels. In addition, increases in the activity of enzymes were also observed: malic, glucose-6-phosphate dehydrogenase, and ATP-citrate lyase, in addition to an increase in the PPARγ content. The results show the occurrence of the futile creatine cycle in ingWAT, and that the increase in the relative mass may be due to an increase in de novo fatty acid synthesis.

Review of Decreased IL-6 Levels in SOPK-Insulin Resistant Rats fed a Low Carb High Protein Diet

Polycystic ovary syndrome with insulin resistance (SOPK-RI) is caused among endocrine disorders with an incidence rate of 5-10% that occurs in women of reproductive age. Characteristics of polycystic ovary syndrome are found anovulation, hyperandrogens, polycystic ovarii and impaired insulin sensitivity involving proinflammatory increases in several inflammatory cytokines including interleukin-6 (IL-6). Increased inflammatory cytokines in women with SOPK-RI found health problems there is fat accumulation in adipocyte tissue such as in an obese person, metabolic syndrome and type 2 diabetes. The purpose of this study was to determine the effect of a low-carbohydrate high-protein diet on changes in IL-6 levels in SOPK-RI model mice. Laboratory experimental research, namely post test only control group design. Consisting of three groups, namely, the negative control group (K-) as a normal group did not get treatment; The positive control group (K+) of the SOPK-insulin resistance model mice were given standard feed, and the treatment group (P) of the SOPK-insulin resistance model mice were given a low-carbohydrate high-protein diet (CTR) with a composition of 40% carbohydrate and 30% protein. The study lasted for 48 days, using serum ELISA examination on IL-6 levels. The average results of IL-6 levels, namely the K- = 0.358 group, K+ = 0.387 and P = 0.442 and obtained different IL-6 levels of significance value p = 0.002 with a low-carbohydrate high-protein diet in SOPK - RI rats showed a significant difference (p &lt; 0.05) between the control group and the treatment group. Significantly reduced IL-6 levels in SOPK-RI model mice. A low-carb, high-protein diet may be considered as a dietary modality in women with SOPK-insulin resistance. Further research is needed to better determine the other modulators involved in this mechanism in more detail.

Chitosan-Based Sustained Expression of Sterol Regulatory Element-Binding Protein 1a Stimulates Hepatic Glucose Oxidation and Growth in Sparus aurata.

The administration of a single dose of chitosan nanoparticles driving the expression of sterol regulatory element-binding protein 1a (SREBP1a) was recently associated with the enhanced conversion of carbohydrates into lipids. To address the effects of the long-lasting expression of SREBP1a on the growth and liver intermediary metabolism of carnivorous fish, chitosan-tripolyphosphate (TPP) nanoparticles complexed with a plasmid expressing the N terminal active domain of hamster SREBP1a (pSG5-SREBP1a) were injected intraperitoneally every 4 weeks (three doses in total) to gilthead sea bream (Sparus aurata) fed high-protein-low-carbohydrate and low-protein-high-carbohydrate diets. Following 70 days of treatment, chitosan-TPP-pSG5-SREBP1a nanoparticles led to the sustained upregulation of SREBP1a in the liver of S. aurata. Independently of the diet, SREBP1a overexpression significantly increased their weight gain, specific growth rate, and protein efficiency ratio but decreased their feed conversion ratio. In agreement with an improved conversion of dietary carbohydrates into lipids, SREBP1a expression increased serum triglycerides and cholesterol as well as hepatic glucose oxidation via glycolysis and the pentose phosphate pathway, while not affecting gluconeogenesis and transamination. Our findings support that the periodical administration of chitosan-TPP-DNA nanoparticles to overexpress SREBP1a in the liver enhanced the growth performance of S. aurata through a mechanism that enabled protein sparing by enhancing dietary carbohydrate metabolisation.

Faecal metabolome responses to an altered dietary protein:carbohydrate ratio in adult dogs

High-protein diets may aid weight loss and weight maintenance programs in both humans and dogs, although the effect of dietary protein levels on gut metabolism and functionality has not been studied in depth. The current study aimed to investigate the effect of an altered dietary protein:carbohydrate ratio on gut function in adult dogs by means of faecal metabolomic fingerprinting. More specifically, functional metabolic differences in dogs fed a high-protein/low-carbohydrate (HPLC) vs. low-protein/high-carbohydrate (LPHC) diet were studied by equally allocating twelve clinically healthy (6 lean and 6 obese) Beagles into two groups in a cross-over design, with each group receiving two isocaloric diets for four weeks. The faecal metabolome revealed that different protein:carbohydrate ratio can influence host and/or gut microbiome metabolism and function, while no effect was observed on the body condition. Targeted analysis demonstrated that the HPLC diet significantly increased the concentration of indole, spermidine, and pipecolinic acid and decreased the concentration of azelaic acid, D-fructose, mannose, and galactose (p < 0.05). Multivariate modelling (OPLS-DA) of the untargeted faecal metabolome revealed distinctly different metabolomic profiles following the HPLC vs. LPHC diet, with 18 altered pathways. The HPLC diet influenced amino acid and lipid metabolism, potentially promoting weight loss and immune function, whereas the LPHC diet affected carbohydrate fermentation and may promote anti-oxidative function.

A Low-Protein, High-Carbohydrate Diet Exerts a Neuroprotective Effect on Mice with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson's Disease by Regulating the Microbiota-Metabolite-Brain Axis and Fibroblast Growth Factor 21.

Parkinson's disease (PD) is closely linked to lifestyle factors, particularly dietary patterns, which have attracted interest as potential disease-modifying factors. Eating a low-protein, high-carbohydrate (LPHC) diet is a promising dietary intervention against brain aging; however, its protective effect on PD remains elusive. Here, we found that an LPHC diet ameliorated 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced motor deficits, decreased dopaminergic neuronal death, and increased the levels of striatal dopamine, serotonin, and their metabolites in PD mice. Levels of fibroblast growth factor 21 (FGF-21), a member of the fibroblast growth factor family, were elevated in PD mice following LPHC treatment. Furthermore, the administration of FGF-21 exerted a protective effect on MPTP-induced PC12 cells, similar to the effect of an LPHC diet in MPTP-induced mice. Sequencing of the 16S rDNA from fecal microbiota revealed that an LPHC diet normalized the gut bacterial composition imbalance in PD mice, as evidenced by the increased abundance of the genera Bifidobacterium, Ileibacterium, Turicibacter, and Blautia and decreased abundance of Bilophila, Alistipes, and Bacteroides. PICRUSt-predicted fecal microbiome function revealed that an LPHC diet suppressed lipopolysaccharide biosynthesis and the citrate cycle (TCA cycle), biosynthesis of ubiquinone and other terpenoid-quinones, and oxidative phosphorylation pathways caused by MPTP, and enhanced the biosynthesis of amino acids, carbohydrate metabolism, and biosynthesis of other secondary metabolites. A nonmetabolomic analysis of the serum and feces showed that an LPHC diet significantly increased the levels of aromatic amino acids (AAAs), including tryptophan, tyrosine, and phenylalanine. In addition, an LPHC diet elevated the serum concentrations of bile acids (BAs), particularly tauroursodeoxycholic acid (TUDCA) and taurine. Collectively, our current findings point to the potential mechanism of administering an LPHC diet in attenuating movement impairments in MPTP-induced PD mice, with AAAs, microbial metabolites (TUDCA and taurine), and FGF-21 as key mediators along the gut-microbiota-brain axis.

Temperature- and Diet-Induced Plasticity of Growth and Digestive Enzymes Activity in Spongy Moth Larvae.

Temperature and food quality are the most important environmental factors determining the performance of herbivorous insects. The objective of our study was to evaluate the responses of the spongy moth (formerly known as the gypsy moth) [Lymantria dispar L. (Lepidoptera: Erebidae)] to simultaneous variation in these two factors. From hatching to the fourth instar, larvae were exposed to three temperatures (19 °C, 23 °C, and 28 °C) and fed four artificial diets that differed in protein (P) and carbohydrate (C) content. Within each temperature regime, the effects of the nutrient content (P+C) and ratio (P:C) on development duration, larval mass, growth rate, and activities of digestive proteases, carbohydrases, and lipase were examined. It was found that temperature and food quality had a significant effect on the fitness-related traits and digestive physiology of the larvae. The greatest mass and highest growth rate were obtained at 28 °C on a high-protein low-carbohydrate diet. A homeostatic increase in activity was observed for total protease, trypsin, and amylase in response to low substrate levels in the diet. A significant modulation of overall enzyme activities in response to 28 °C was detected only with a low diet quality. A decrease in the nutrient content and P:C ratio only affected the coordination of enzyme activities at 28 °C, as indicated by the significantly altered correlation matrices. Multiple linear regression analysis showed that variation in fitness traits in response to different rearing conditions could be explained by variation in digestion. Our results contribute to the understanding of the role of digestive enzymes in post-ingestive nutrient balancing.

Abstract #1408210: Glycogen Storage Disease Type III Presenting as Seizure in an African American Male

Glycogen is the stored form of glucose which serves as a buffer for glucose needs. It is formed in periods of dietary carbohydrate loading and broken down when glucose demand is high or dietary availability is low. The main role of glycogen in the liver is to store glucose for release to tissues that are unable to synthesize significant amounts during fasting. In the muscle, glycogen serves as the primary source of energy for high-intensity muscle activity by providing substrates for the generation of adenosine triphosphate. Glycogen storage diseases (GSD) are rare inborn errors of glycogen metabolism that result from mutations in genes involved in glycogen storage. The age of onset varies from in utero to adulthood. The most affected organs are the liver and muscle where glycogen is abundant. Liver manifestations include hypoglycemia and hepatomegaly while muscle manifestations include cramps, exercise intolerance, easy fatigability, and progressive weakness. GSD III is due to an abnormality in the Amylo-Alpha-1, 6-Glucosidase, 4-Alpha-Glucanotransferase (AGL) gene causing deficiency of the glycogen debrancher enzyme. It is inherited as an autosomal recessive trait. Estimated prevalence is 1:100,000. It is characterized by variable liver, cardiac muscle and skeletal involvement. GSD IIIa is present in about 85% of affected individuals and manifests with liver and muscle involvement. GSD IIIb is in about 15 % of affected individuals with liver involvement only. The patient was born to a 35-year-old African American mother at 38 weeks gestation. Labor and delivery were uncomplicated. Initial labs showed blood glucose of 38 mg/dl for which he was placed on a hypoglycemia protocol. Breastfeeding was started successfully with no more noted hypoglycemia and he was discharged home. At 11 months he was taken to the ER after a witnessed tonic clinic seizure. Blood glucose was noted to be 24 mg/dl. He was managed with hypoglycemia protocol and Pediatric Endocrinology team consulted. Labs showed elevated liver enzymes, creatinine kinase and cholesterol with ALP 1101 units/L, AST 1822 units/L, ALT 1148 units/L, CK 783 units/L, total cholesterol 223mg/dl, triglyceride 249 mg/dl and HDL 30 mg/dl. Abdominal US showed hepatomegaly and echo showed left ventricular and septal hypertrophy. GSD was suspected so genetic testing was done and showed 2 frameshift mutations in the AGL gene confirming GSD Type IIIa. He was started on a low carbohydrate high protein diet together with corn starch with minimal hypoglycemia episodes. He has been closely followed at the pediatric Endocrinology clinic and is now 17 years old. He has a DEXCOM continuous glucose monitor. Most recent labs show some improvement in liver enzymes and lipids. Both of his parents are positive for the GSD III trait. Unexplained hypoglycemia warrants a thorough work up as highlighted in this case. Most of the severe forms of GSDs are diagnosed in childhood but some mild forms can be diagnosed in adulthood. Both pediatric and adult endocrinologists should have sufficient knowledge on the diagnosis and management of GSDs.

Comparison of the Effect of a Protein-Free and Restricted High Protein—Low Carbohydrate Diet on Ventricular Myosin ATPase Activity and Isomyosin Profile in Young Rats: Evidence That Protein-Depleted Animals Are Euthyroid

Young rats fed a protein-deficient diet have elevated total triiodothyronine (T3) levels in spite of decreased skeletal muscle protein turnover. Interpretation of the thyroid status of these animals is complicated by increased T3 binding by serum proteins. Free T3 levels ranging from normal to low and decreased resting oxygen consumption have been reported. To investigate the thyroid status of animals fed a protein-free diet, ventricular myosin ATPase activity and isomyosin profile have been used as an index of thyroid hormone activity. The effect of the protein-free diet has been compared to a restricted high protein-low carbohydrate diet, which causes clear evidence of decreased thyroid hormone effect. After 28 d, calcium-activated myosin ATPase activity was 1.50 ± 0.05 µmol P1/(mg protein · min) in animals fed the basal diet, 1.16 ± 0.03 µmol P1/ (mg protein · min) in animals fed the restricted high protein-low carbohydrate diet and 1.48 ± 0.04 µmol P1/(mg protein · min) in animals fed the protein-free diet. In addition, a shift in isomyosin content with the appearance of V2 and V3 isomyosins occurred with the restricted high protein-low carbohydrate diet but not the protein-free diet. The failure of the protein-depleted rats to decrease myosin ATPase activity and alter isomyosin content suggests that they are euthyroid.

Nutritional geometry framework of sucrose taste in Drosophila

Dietary protein (P) and carbohydrate (C) have a major impact on the sweet taste sensation. However, it remains unclear whether the balance of P and C influences the sweet taste sensitivity. Here, we use the nutritional geometry framework (NGF) to address the interaction of protein and carbohydrates on sweet taste using Drosophila as a model. Our results reveal that high-protein, low-carbohydrate (HPLC) diets sensitize to sweet taste and low-protein, high-carbohydrate (LPHC) diets desensitize sweet taste in both male and female flies. We further investigate the underlying mechanisms of the effects of two diets on sweet taste using RNA sequencing. When compared to the LPHC diet, the mRNA expression of genes involved in the metabolism of glycine, serine, and threonine is significantly upregulated in the HPLC diet group, suggesting these amino acids may mediate sweet taste perception. We further find that sweet sensitization occurs in flies fed with the LPHC diet supplemented with serine and threonine. Our study demonstrates that sucrose taste sensitivity is affected by the balance of dietary protein and carbohydrates possibly through changes in serine and threonine.

Characterisation of the Paternal Influence on Intergenerational Offspring Cardiac and Brain Lipid Homeostasis in Mice.

There is growing evidence that poor paternal diet at the time of conception increase the risk of offspring developing a range of non-communicable metabolic diseases, such as obesity, diabetes and cardiovascular disease, in adulthood. We hypothesise that a paternal low protein-high carbohydrate diet perturbs offspring tissue lipid abundance through both sperm and seminal plasma-mediated mechanisms. To test our hypothesis, we fed male C57BL/6 mice either a control normal protein diet (NPD; 18% protein) or an isocaloric low protein diet (LPD; 9% protein) for a minimum of 8 weeks. We generated offspring through artificial insemination, in combination with vasectomised male mating. Using this approach, we derived offspring from either NPD or LPD sperm but in the presence of NPD or LPD seminal plasma. Using high resolution mass-spectrometry, we found that offspring derived from either LPD sperm or seminal fluid displayed perturbed cardiac and brain lipid abundance from just three weeks of age, typically associated with the altered abundance of tissue triglycerides. We also observed the differential sex-specific patterns of lipids between the control and experimental offspring's hearts and brains. These observations indicate that poor paternal diet at the time of conception affects offspring cardiac and brain lipid profiles in an age-, sex- and generation-specific manner.

Isocaloric Diets with Different Protein-Carbohydrate Ratios: The Effect on Sleep, Melatonin Secretion and Subsequent Nutritional Response in Healthy Young Men.

This study aimed to determine the short-term effect of two isocaloric diets differing in the ratio of protein−carbohydrate on melatonin levels, sleep, and subsequent dietary intake and physical activity in healthy young men. Twenty-four healthy men took part in a crossover design including two sessions of three days on isocaloric diets whether high-protein, low-carbohydrate (HPLC) or low-protein, high-carbohydrate (LPHC) followed by 24-h free living assessments. Sleep was measured by ambulatory polysomnography pre-post-intervention. Melatonin levels were assessed on the third night of each session on eight-point salivary sampling. Physical activity was monitored by accelerometry. On day 4, participants reported their 24-h ad-libitum dietary intake. LPHC resulted in better sleep quality and increased secretion of melatonin compared to HPLC. A significant difference was noted in sleep efficiency (p < 0.05) between the two sessions. This was mainly explained by a difference in sleep onset latency (p < 0.01) which was decreased during LPHC (PRE: 15.8 ± 7.8 min, POST: 11.4 ± 4.5 min, p < 0.001). Differences were also noted in sleep staging including time spent on REM (p < 0.05) and N1 (p < 0.05). More importantly, REM latency (PRE: 97.2 ± 19.9 min, POST 112.0 ± 20.7 min, p < 0.001) and cortical arousals (PRE: 7.2 ± 3.9 event/h, POST 8.5 ± 3.3 event/h) increased in response to HPLC diet but not LPHC. On day 4, 24-h ad-libitum energy intake was higher following HPLC compared to LPHC (+64 kcal, p < 0.05) and explained by increased snacking behavior (p < 0.01) especially from carbohydrates (p < 0.05). Increased carbohydrates intake was associated with increased cortical arousals.

LCHP Diet Enriched with Cholesterol Promotes Non-Alcoholic Fatty Liver Disease in Wistar Rats

The aim of this study was to analyze the effect of a low-carbohydrate–high-protein diet, enriched with cholesterol (LCHPch), on body weight, lipid metabolism, as well as kidney and liver function in rats. Wistar rats (N = 18, male) were randomly allocated into experimental groups and fed a modified AIN-93G diet with the addition of 1% cholesterol (AINch, WDch and LCHPch diets) for 8 weeks. Despite the lack of significant differences in the final body weight and liver weight of animals, the kidneys of rats in the LCHPch group were considerably heavier compared to the control group. Serum total cholesterol and the sum of low- and very-low-density fractions of cholesterol as well as ALT activity were significantly increased in the LCHPch rats in comparison to the AINch group. Simultaneously, the highest content of liver fat was obtained for animals from LCHPch group. It was also shown that both WDch and LCHPch diets significantly changed fatty acid profile in the adipose tissue of rats compared to control, with a significant increase in SFA and MUFA and a decrease in PUFA. Non-alcoholic fatty liver disease was observed in rats fed not only WDch but also LCHPch diets. The detailed mechanism still needs to be investigated to prevent the organism from the harmful effects of macronutrient dietary imbalance.

Effects of Low Protein-High Carbohydrate Diet during Early and Late Pregnancy on Respiratory Quotient and Visceral Adiposity.

Background Low Protein-High Carbohydrate (LPHC) diet during pregnancy is considered a nutritional and health problem related to the development of maternal metabolic alterations, such as fatty liver and obesity in the perinatal and postnatal period. It is known that increase in visceral adiposity tissue (VAT) modulates maternal metabolic rate, with the respiratory quotient (RQ) being a parameter related to that variable; however, it is unknown whether LPHC intake during pregnancy affects the VAT and the RQ. In this study, we examine if consumption of LPHC during pregnancy modifies the VAT and RQ in early and late periods of pregnancy. Methods This is a longitudinal and cross-sectional study with Wistar rats during gestation (G) (3, 8, 15, and 20) and nonpregnant rats. Rats were fed with a control diet with 63/18% carbohydrate/protein and an experimental diet with 79/6% carbohydrate/protein. We studied water and food consumption and metabolic parameters such as RQ and energy expenditure (EE), calculated by indirect calorimetry. In the cross-sectional study, we determined visceral fat, as well as the concentration of free fatty acids, insulin, glucose, and lipid profile in serum. Results Nonpregnant rats with LPHC intake decreased significantly in VAT (86%) and the RQ (18%); in pregnant rats in early (8G) and late pregnancy (15G) in LPHC diet, both parameters (VAT and RQ) (25%-92%) increased during light time. When comparing time points during pregnancy in the control and LPHC groups, the RQ increased in 15G during daytime compared to 8G during the night period (17 and 5%, respectively). In late pregnancy, LPHC intake and triacylglyceride levels increased and cholesterol and glucose decreased (45 and 26%, respectively), in comparison to nonpregnant rats. Conclusions LPHC intake in nonpregnant rats decreases the RQ and VAT. Interestingly, the opposite occurs in early pregnancy: the RQ and VAT increased, and this correlates with free fatty acid (FFA) levels. The increase in RQ and VAT during light time in early pregnancy increased mobilization of carbohydrate and protein metabolism. These results suggest that LPHC intake during pregnancy increases the glucose metabolism as a compensatory mechanism for energy needs in the fetus and the mother in early pregnancy.

Hyperphagia and hyperleptinemia induced by low-protein, high-carbohydrate diet is reversed at a later stage of development in rats.

This study investigated whether increased food intake after 15 days of low-protein, high-carbohydrate (LPHC) and its normalization in the later period of development change the content of key proteins related to leptin or adiponectin signaling in the hypothalamus. Male rats were divided into five groups: Control groups received a control diet (17% protein, 63% carbohydrate) for 15 (C15) or 45 (C45) days; LPHC groups received an LPHC diet (6% protein, 74% carbohydrate) for 15 (LPHC15) or 45 (LPHC45) days; and Reverse group (R): received LPHC diet for 15 days followed by control diet for another 30 days. The LPHC15 group showed increased adiposity index, leptin level, and adiponectin level, as well as decreased the leptin receptor (ObRb) and pro-opiomelanocortin (POMC) content in the hypothalamus compared with the C15 group. LPHC diet for 45 days or diet reversion (R group) rescued these alterations, except the adiponectin level in LPHC45 rats, which was higher. In summary, LPHC diet reduced hypothalamic leptin action by diminishing ObRb and POMC levels, leading to hyperphagia and adiposity body. Medium-term administration of LPHC diet or reverting to control diet restored the levels of these proteins, thereby improving body lipid mass rearrangement in adulthood.

Hepatic Global DNA Hypomethylation Phenotype in Rainbow Trout Fed Diets Varying in Carbohydrate to Protein Ratio

BackgroundA high carbohydrate–low protein diet can induce hepatic global DNA hypomethylation in trout. The mechanisms remain unclear. ObjectivesWe aimed to investigate whether an increase in dietary carbohydrates (dHCs) or a decrease in dietary proteins (dLPs) can cause hepatic global DNA hypomethylation, as well as explore the underlying mechanisms in trout. MethodsTwo feeding trials were conducted on juvenile males, both of which involved a 4-d fasting and 4-d refeeding protocol. In trial 1, trout were fed either a high protein–no carbohydrate [HP-NC, protein 60% dry matter (DM), carbohydrates 0% DM] or a moderate protein–high carbohydrate (MP-HC, protein 40% DM, carbohydrates 30% DM) diet. In trial 2, fish were fed either a moderate protein–no carbohydrate (MP-NC, protein 40% DM, carbohydrates 0% DM), an MP-HC (protein 40% DM, carbohydrates 30% DM), or a low protein–no carbohydrate (LP-NC, protein 20% DM, carbohydrates 0% DM) diet to separate the effects of dHCs and dLPs on the hepatic methylome. Global CmCGG methylation, DNA demethylation derivative concentrations, and mRNA expression of DNA (de)methylation-related genes were measured. Differences were tested by 1-factor ANOVA when data were normally distributed or by Kruskal–Wallis nonparametric test if not. ResultsIn both trials, global CmCGG methylation concentrations remained unaffected, but the hepatic 5-mdC content decreased after refeeding (1–3%). The MP-HC group had 3.4-fold higher hepatic 5-hmdC and a similar 5-mdC concentration compared with the HP-NC group in trial 1. Both MP-HC and LP-NC diets lowered the hepatic 5-mdC content (1–2%), but only the LP-NC group had a significantly lower 5-hmdC concentration (P < 0.01) compared with MP-NC group in trial 2. ConclusionsdHC and dLP independently induced hepatic global DNA demethylation in trout. The alterations in other methylation derivative concentrations indicated the demethylation process was achieved through an active demethylation pathway and probably occurred at non-CmCGG sites.