Dietary supplementation of myo-inositol for preventing fatty liver disease by altering hepatic epigenetic modifications in the transcribed regions of Fasn and Elovl6.

Dietary supplementation with myo-inositol reduces high-fructose diet-induced hepatic ChREBP binding and acetylation of histones H3 and H4 on the Elovl6 gene in rats

Changes in growth performance, haematological parameters, hepatopancreas histopathology and antioxidant status of pacific white shrimp (Litopenaeus vannamei) fed oxidized fish oil: Regulation by dietary myo-inositol

The impaired Na(+)-K(+)-ATPase activity in peripheral nerve from diabetic rats is prevented by dietary myo-inositol (MI) supplementation in vivo and corrected by protein kinase C (PKC) agonists in vitro, suggesting that PKC may mediate the effects of nerve MI depletion on Na(+)-K(+)-ATPase activity. However, little is known about the effect of diabetes on PKC activity or peptide in rat peripheral nerve. Therefore, the effect of streptozocin-induced diabetes and dietary MI supplementation on the activity and distribution of PKC in rat sciatic nerve homogenates and cytosolic and particulate fractions was explored with histone phosphorylation assay and Western-blot analysis. PKC activity but not peptide was selectively decreased in the cytosolic fraction by streptozocin-induced diabetes, and this abnormality was partially corrected by dietary MI supplementation. These results suggest that altered MI metabolism may affect nerve PKC specific activity, and this alteration may play a role in reduced Na(+)-K(+)-ATPase activity and blunted regenerative response in diabetic nerve.

New insights into the influence of myo-inositol on carbohydrate metabolism during osmoregulation in Nile tilapia (Oreochromis niloticus).

Regulatory role of myo-inositol in the ovarian development of female Chinese mitten crab (Eriocheir sinensis)

Growth, osmotic response and transcriptome response of the euryhaline teleost, Oreochromis mossambicus fed different myo-inositol levels under long-term salinity stress

Myo-inositol improves osmoregulation by promoting lipid utilization in Nile tilapia (Oreochromis niloticus)

Simple SummaryRecently, the price escalation of fishmeal has made aquaculture nutritionists to consider using carbohydrate in aquafeed to spare the use of dietary protein. However, the high carbohydrate diet could induce lipid metabolism disorder, impair antioxidant capacity, reduce nonspecific immunity and decrease resistance to a pathogen in farmed fish. Myo-inositol is regarded as a vitamin-like essential nutrient for most aquatic animals. Previous studies have shown that dietary supplementation with myo-inositol can reduce lipid accumulation in tissues and decrease the chance of becoming a fatty liver. To explore the mechanism of myo-inositol on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia, six diets contained either low carbohydrate (30%) or high carbohydrate (45%) with three levels of myo-inositol supplementation (0, 400 and 1200 mg/kg diet) to each level of the carbohydrate diet. After an 8-week trial, the result showed that additive myo-inositol in the diet could significantly improve the growth performance and increase the crude protein content of fish. The addition of myo-inositol could effectively decrease the lipid accumulation induced by the high carbohydrate diet by accelerating the transportation of cholesterol back to the liver and promoting the lipid decomposition.This study investigated the effect of dietary myo-inositol (MI) on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia (Oreochromis niloticus). Six diets contained either low carbohydrate (LC 30%) or high carbohydrate (HC 45%) with three levels of MI supplementation (0, 400 and 1200 mg/kg diet) to each level of the carbohydrate diet. After an 8-week trial, the fish fed 400 mg/kg MI under HC levels had the highest weight gain and fatness, but the fish fed 1200 mg/kg MI had the lowest hepatosomatic index, visceral index and crude lipid in the HC group. The diet of 1200 mg/kg MI significantly decreased triglyceride content in the serum and liver compared with those fed the MI supplemented diets regardless of carbohydrate levels. Dietary MI decreased triglyceride accumulation in the liver irrespective of carbohydrate levels. The content of malondialdehyde decreased with increasing dietary MI at both carbohydrate levels. Fish fed 1200 mg/kg MI had the highest glutathione peroxidase, superoxide dismutase, aspartate aminotransferase and glutamic-pyruvic transaminase activities. The HC diet increased the mRNA expression of key genes involved in lipid synthesis (DGAT, SREBP, FAS) in the fish fed the diet without MI supplementation. Dietary MI significantly under expressed fatty acid synthetase in fish fed the HC diets. Moreover, the mRNA expression of genes related to lipid catabolism (CPT, ATGL, PPAR-α) was significantly up-regulated with the increase of dietary MI levels despite dietary carbohydrate levels. The gene expressions of gluconeogenesis, glycolysis and MI biosynthesis were significantly down-regulated, while the expression of the pentose phosphate pathway was up-regulated with the increase of MI levels. This study indicates that HC diets can interrupt normal lipid metabolism and tend to form a fatty liver in fish. Dietary MI supplement can alleviate lipid accumulation in the liver by diverging some glucose metabolism into the pentose phosphate pathway and enhance the antioxidant capacity in O. niloticus.

This study was conducted to determine the optimal dietary myo-inositol (MI) requirement of juvenile hybrid sturgeon (Acipenser baerii ♀ × A. schrenckii ♂). Fish with an initial average body weight of 28.28 ± 0.41 g were randomly divided into six groups with three repetitions in each group and fed the experimental diets with different graded MI concentrations (70.2, 130.0, 270.2, 443.0, 1,096.6 and 1997.3 mg/kg) three times per day for 12 weeks. The results showed that with the increase in dietary MI level from 70.2 mg/kg to 443.0 mg/kg, weight gain (WG) was increased significantly (p < .05); however, when the MI level was further increased, there was no significant difference in weight gain rate (WG) over time (p > .05). Specific growth rate (SGR) showed a similar trend. The feed conversion ratio (FCR), survival rate (SR), hepatosomatic index (HSI), viscerasomatic index (VSI) and condition factor (CF) were not affected by dietary MI supplementation (p > .05). Dietary MI did not affect whole-body and muscle crude protein and ash content (p > .05), while dietary MI significantly affected the muscle and whole-body crude lipid and moisture content (p < .05). Moreover, serum triglyceride (TG), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were decreased by increasing dietary MI levels. Total antioxidant capacity (T-AOC), malonic dialdehyde (MDA) and superoxide dismutase (SOD) activities in the liver were also affected by the dietary MI (p < .05). In summary, this study indicated that the optimal dietary MI requirement for juvenile hybrid sturgeon (Acipenser baerii ♀ × A. schrenckii ♂) was 335.84 mg/kg and 590.65 mg/kg based on the maximum WG and liver MI accumulation indices respectively.

Dietary supplementation with myo-inositol reduces hepatic triglyceride accumulation and expression of both fructolytic and lipogenic genes in rats fed a high-fructose diet

This study was aimed at examining the essentiality and requirement of inositol for Olive flounder, Paralichthys olivaceus. Six casein–gelatin-based semi-purified diets were formulated to contain five different levels of myo-inositol (MI) (designated as M0, M0+, M200, M400, M800 and M1600 for 0, 0+antibiotic, 200, 400, 800 and 1600 mg kg−1 respectively). After 20 weeks of a long-term feeding trial, fish (initial body weight, 10 g) fed the M800 diet showed significantly increased growth performances and survival. Liver lipid concentration tended to decrease as the dietary MI increased, although there was no significant difference among all treatments. Polyunsaturated fatty acid in the liver of the fish fed the diets containing high levels (M1600) of MI was significantly increased. Hepatic inositol concentration of the fish was significantly increased by dietary MI supplementation. The intestinal biosynthesis of inositol by microflora seemed to be insufficient to prevent growth retardation in juvenile Olive flounder. The optimum level of dietary MI for juvenile Olive flounder was found to be 617 mg kg−1 based on weight gain in a broken-line regression model. This finding indicates that MI supplementation is required at a concentration of at least 617 mg kg−1 to maximize the growth performances and to prevent abnormal lipid metabolism.

Toxicity of chronic copper exposure on Chinese mitten crab (Eriocheir sinensis) and mitigation of its adverse impact by myo-inositol

Myo-inositol (MI) plays key roles in cellular signaling, membrane structure, and metabolic regulation, with its effects in poultry primarily explored through direct dietary MI supplementation. In this study, we aimed to assess the effects of in ovo MI administration on post-hatch performance and metabolism of broiler chickens. A total of 480 fertilized Ross 308 eggs were divided into four groups and, on day 17 of incubation, were injected with 12 μmol/mL MI (MI 12), 24 μmol/mL MI (MI 24), 0.9% saline (positive control, PC), or left non-injected (negative control, NC). After hatching, broilers were group-housed in floor pens (8 pens per treatment), with 12 birds per pen, and fed a standard diet for 35 days. At d 35, one bird per pen was slaughtered, sex was identified, and blood and tissues were collected to assess MI concentrations, the expression of inositol monophosphatase 1 (IMPase 1) and myo-inositol oxygenase (MIOX), and plasma metabolite profiles. There was no adverse effect of MI in ovo administration on hatchability and body weight (BW) of hatchlings. During the growing period, BW was lower in MI-injected groups from day 14 onward, along with reduced average daily weight gain; however, no differences were observed in the feed conversion ratio. The survival rate was higher in MI-injected groups during days 0-21, with a positive trend until the end of the experiment. MI concentrations in plasma and tissues, along with the expression of IMPase 1 and MIOX, were not altered by treatment. Plasma metabolomics revealed higher C2 and C9 acylcarnitines, threonine, and sarcosine, along with lower serotonin, and notable changes in phosphatidylcholines and sphingolipids in MI-injected versus no-MI groups, potentially reflecting alterations in mitochondrial β-oxidation pathways, diacylglycerol-associated signaling, amino-acid-related metabolism, and peripheral serotonin metabolism. Sex-specific differences in plasma MI and metabolite profiles were detected, with male birds demonstrating reduced plasma MI concentrations, Fisher ratio, and carnosine levels, indicative of a metabolic state possibly associated with higher anabolic pressure or subclinical inflammatory activation. These findings highlight the potential of in ovo MI administration to induce subtle but persistent metabolic reprogramming and underscore the need for further studies to clarify its long-term consequences for metabolic resilience and performance in both sexes.

Dietary myo-inositol effect on sugar cataractogenesis.

Nerve conduction impairment in experimental diabetes has been empirically but not mechanistically linked to altered nerve myo-inositol metabolism. The phospholipid-dependent membrane-bound sodium-potassium ATPase provides a potential mechanism to relate defects in diabetic peripheral nerve myo-inositol-phospholipid metabolism, impulse conduction, and energy utilization. Therefore, the effect of streptozocin-induced diabetes mellitus and dietary myo-inositol supplementation on rat sciatic nerve sodium-potassium ATPase was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 4-wk streptozocin diabetic rats and age-matched controls either fed a standard or 1% myo-inositol supplemented diet. The sodium-potassium ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Diabetes reduced the composite ATPase activity recovered in crude homogenates of sciatic nerve. The 40% reduction in the sodium-potassium ATPase was selectively prevented by 1% myo-inositol supplementation (which preserved normal nerve conduction). Thus, in diabetic peripheral nerve, abnormal myo-inositol metabolism is associated with abnormal sodium-potassium ATPase activity. The mechanism of the effect of dietary myo-inositol to correct diabetic nerve conduction may be through changes in a sodium-potassium ATPase, possibly via changes in myo-inositol-containing phospholipids.