Keto Means
Keto Means
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Reversion to regular diet with alternate day fasting can cure grade-I non-alcoholic fatty liver disease (NAFLD) in high-fructose-intake-associated metabolic syndrome.
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Read More »Understanding the pathophysiology of MetS is essential, if therapy of MetS-associated NAFLD is to be considered. Pathophysiology of MetS is multifactorial with the unhealthy lifestyle a strongly predisposing factor [42]. Lifestyle aspects include nutrition, physical activity, sleeping hours, smoking, alcohol intake, working hours, hours of watching television, afternoon napping, and social life with friends [42]. Healthy nutrition as described by Mattson et al. [43] includes healthy diet (Mediterranean diet), intake of nutraceuticals, and dietary constriction in the form of caloric restriction or intermittent fasting—defined as periods of unrestricted feeding alternating with periods of caloric restriction. Unhealthy nutrition is an aspect of unhealthy life style and includes intake of foods with high caloric content, high glycemic index, high content of fructose, high percentage of saturated to polyunsaturated fat, low fruit and vegetable fiber content, as well as irregular eating [44,45,46,47]. Garralda-Del-Villar et al. [42] hypothesized that higher adherence to the healthy lifestyle is associated with a lower risk of developing MetS. In the present work, MetS was induced by applying one aspect of unhealthy lifestyle namely unhealthy nutrition in the form of excess fructose intake both in food and drink which mimic the increasing intake of this sweetener in foods and drinks by humans [48]. Fructose content in diet and drink of MS group was equal to starch content in the control rat diet. The present study was planned to investigate the ability of dietary intervention in the form of reversion to normal diet—with or without adoption of a healthy dietary pattern like zero-calorie intermittent fasting—to cure MetS-associated steatosis which is the hallmark of diagnosis of NAFLD. The results of the present study revealed that 8 weeks of high fructose diet (HFD) was able to induce features of MetS in M rats as evidenced by the significant increase in WC, PG, and AUC as well as the significant decrease of HDL-C compared to control rats. Additionally, in comparison to their initial values, M group presented a significant increase in WC, FBS, PG, AUC, and TG associated with a significant decrease in HDL-C after 8 weeks of HFD. According to the criteria of harmonizing definition of Alberti et al. [1], M rats, in the present study, showed two criteria of MetS, namely high FBG and low HDL-C, skipping the normal cutoff values of FBG (> 100 mg%), and HDL-C (< 40 mg/dl). Although the cutoff value of WC in the previous definition is not applicable to rats, yet the significant increase in WC in M compared to control rats could be considered the third criterion needed to diagnose MetS in this group. This was consistent with the study of Di Luccia et al. [49], on Sprague-Dawley rats which developed the same MetS criteria, developed in the present study, after 8 weeks of HFD. Moreover, histopathological study of M rats’ livers showed liver steatosis (score-4), hepatocyte ballooning (score-1), and lobular inflammation (score-1), making activity score-2 which both indicate the development of grade-1 NAFLD according to the score of Mendler et al. [40], and highlighting the early emergence of steatohepatitis. Thus, the results of M rats in the present study confirm the close association between unhealthy nutrition in the form of excess fructose intake, MetS, and steatohepatitis and agree with the findings of Mamikutty et al. [50]. At the end of the study, MS rats showed amelioration of two criteria of MetS (VFW, VFW/BW, and FBG) with HDL-C value remaining below the cutoff value of low HDL-C (< 40 mg/dl) according to Alberti et al. [1]. However, liver derangement was evident in the form of significantly increased LW, LW/BW, and serum ALT as well as decreased serum albumin compared to control rats. In support, histological studies revealed progression of their liver fatty changes from 69 to 82% and hepatocyte ballooning score from to 2 with presence of Mallory bodies. Accordingly, the results of MS group at the end of the study indicate that metabolic perturbation induced by high fructose intake is the determinant of NAFLD disease rather than the MetS criteria. Nutritional intervention, in the present study, namely cessation of fructose intake without caloric restriction in MSRD group, and ADF with continued fructose intake in MSF group resulted in significant amelioration of insulin resistance (serum insulin and HOMA-IR), and dyslipidemia compared to MS rats. The long-term glycemic control parameter (HbA1C) in both groups was declined versus MS rats, approached the control value in both groups and became lower than the normal cutoff value (< 5.7%) according to American diabetes association [51], in MSF group. Such improved glucose homeostasis was further supported by the significant decrease in FBG level at the end of the study versus the 8th week value in both MSRD and MSF groups. Alleviation of insulin resistance and dyslipidemia for 4 weeks, herein, contributed to interruption of the pathogenic circuits that lead to oxidative stress and inflammation, as evidenced by the significant decrease in liver MDA, as well as serum CRP, in both groups versus MS rats, resulting in regression of fatty change and abatement of hepatocyte ballooning. Such remarkable effect was able to significantly relive LW, LW/BW, liver injury (decreased ALT), and improve liver function (increased albumin) in both groups versus MS group. Moreover, hepatic steatosis and steatohepatitis were decreased in both groups versus MS rats as demonstrated by the histological studies. PAS staining of MSRD livers showed increased PAS +ve glycogen granules in zone 1 vacuolated hepatocytes which infer improved insulin resistance in this zone compared to MS group. However, the absence of PAS +ve glycogen granules from zone 3 of MSRD rat livers was in contrast with MS rat livers and might be attributed to either reversal of metabolic zonation of hepatocytes with reversion to regular diet, reversal of insulin resistance with zone 3 hepatocytes becoming more resistant to glycogenic actions of insulin and zone 1 more sensitive to glycogenic actions of insulin with enhanced glucose uptake and glycogenesis in zone 1. The exact changes in oxygen gradient, nutrient flow, and expression of different genes in metabolic syndrome-associated NAFLD should be thoroughly investigated before suggesting a plausible explanation of this alteration in hepatic zonation with reversion to regular diet.
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Read More »MSF hepatocytes showed no PAS +ve glycogen granules throughout the hepatic lobule which might be attributed to enhanced glycogenolysis and suppressed glycogenesis due to the fasting-associated hormonal changes, an observation that was also seen in the MSRDF rat livers. Thus, both diet regimens, in the current work, were able to attenuate the metabolic derangement induced by HFD, alleviating liver damage, hepatic steatosis, steatohepatitis, and conserve liver function. It seems likely that both diet regimens used in the current work, equally and positively affected the insulin resistance, long-term glycemic control, dyslipidemia, serum albumin, and CRP as proved by the non-significant changes in these parameters between MSRD and MSF groups. However, ADF was more effective in lowering the liver oxidative stress and mitigating the hepatocellular damage than reversion to regular rat diet, as manifested by the significant decrease in liver MDA and ALT levels along with a lower score of Mallory bodies as well as hepatocyte ballooning in MSF group versus MSRD rats. Additionally, at the end of the study, the overall obesity parameters (BW) and the visceral obesity parameters (WC) were significantly higher than their matched 8th week values in MSRD group. Also, these parameters together with VFW and VFW/BW were not significantly affected in MSRD group versus controls at the end of the study. These findings indicate that cession of fructose for 4 weeks without caloric restriction neither affected the overall obesity nor the visceral obesity. On the contrary, zero-caloric-intermittent fasting with continued fructose intake, herein, was not only able to significantly decrease the overall and visceral obesity parameters in MSF group at the end of the study period versus their matched values at 8th week, but also, it significantly decreased both in MSF group compared to MS group and MSRD group, becoming even significantly lower than controls. These observations agree with Wan et al. [52], Yang et al. [19], Marinho et al. [53], and Munhoz et al. [54], and denote that caloric restriction by ADF strongly decreased obesity whether overall or visceral, despite the presence of fructose in diet, exceeding the effect of complete cession of fructose in MSRD group. These observations are consistent with Munhoz et al. [54] who found a 35% decrease in total caloric intake and 20.35 % decrease in body weight gain after 12 weeks of ADF in rats. It is to be noted that reversion to regular rat diet or ADF for 4 weeks did not completely abolish the increase in insulin resistance, dyslipidemia, liver oxidative stress, ALT, and the decrease in albumin induced by HFD during the first 8 weeks of the study period as their levels in both MSRD and MSF groups were still significantly different from those of control rats. Likewise, the hepatic steatosis and steatohepatitis did not normalize in both groups. A longer duration of nutritional intervention might be required for full correction if each diet regimen was applied individually. Combination of ADF and reversion to regular rat diet resulted in a synergistic impact on glucose homeostasis parameters, leading to a significant decrease in FBG in MSRDF group versus the MS, MSRD, and MSF group, becoming even significantly lower than controls. This was associated with a remarkable enhancement of glucose clearance with improved glucose tolerance as shown by the significant lower AUC in MSRDF group versus both MSF group and control rats. Furthermore, insulin resistance (HOMA-IR) and long-term glycemic control (HbA1C) were normalized in MSRDF group, as both parameters approached the control values. Furthermore, the parameters of overall obesity and visceral obesity were diminished significantly in MSRDF group compared to MS, MSRD, and control groups. Additionally, combination of the 2 diet regimens significantly improved all lipid profile parameters and attenuated dyslipidemia, liver oxidative stress compared to MS and MSRD rat groups, with CRP and serum albumin still comparable to MSRD group. This was further clarified by the histopathological study of MSRDF rats’ livers which revealed resolution of steatosis with FC score-zero and cure of steatohepatitis. Data of these rats indicate that fasting with reversion to normal diet could cure grade-1 NAFLD. Dyslipidemia was also alleviated in MSRDF group versus MSRD and MSF groups, only TC and LDL-C reached the normal control values, while TG was still significantly higher, and HDL-C was significantly lower. The incomplete correction of lipid parameters in MSRDF to control values might explain the failure of the 2 diet regimens in this group to fully ameliorate the liver oxidative stress, hence the serum albumin level was still significantly lower.
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Read More »Also, of interest was the non-significant changes in obesity parameters, liver MDA, and ALT between MSF and MSRDF group despite their significant decrease in MSRDF versus MSRD group, indicating that caloric restriction by ADF rather than reversion to regular rat diet is responsible for (a) mediating obesity lowering effect and (b) alleviating liver oxidative stress and liver injury in MSRDF group. These observations support our previous assumption that ADF regimen has a dominant effect in alleviating obesity, liver oxidative stress, and liver injury compared to reversion to regular rat diet. Unpredictably, control rats, in the present study, have developed some features of the MetS on the 8th week, and according to the diagnostic criteria of harmonizing definition of Alberti et al. [1], they were found to have 2 criteria out of 3 needed for MetS diagnosis (low HDL-C 37.7 mg/dl and high FBG glucose100.5 mg/dl). Also, at the end of the study, control rats presented a significantly higher WC versus their matched 8th week value together with high FBG (FBG > 100 mg/dl). These changes might be explained by age progression according to Ghezzi et al. [55] who concluded that the aging process induced metabolic disturbances in Wistar rats and that mature rats (12 months old) showed a significant increase in BW, adiposity, hyperglycemia, as well as dyslipidemia compared to young rats. The absence of liver steatosis in control rats, herein, as demonstrated by the histopathological studies makes the diagnosis of MetS in these rats inappropriate according to Panchal and Brown [56] who included liver dysfunction as a MetS criterion for the animal model of MetS to be validated. This study has some limitations including lack of caloric intake estimation and lack of fasting control group. Also, it would be of value to determine the local inflammatory response in the liver tissue by estimating TNF-α and/or TGF-β, and that histopathological study was done for 2 rats in each group and not for all rats which made correlation study between NAFLD grading criteria and other parameters inapplicable.
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