Dietary Lipid Research Articles

Effect of dietary protein to energy ratios on growth, digestive enzyme activity and body composition of captive juvenile spiny lobsters, Panulirus ornatus (Fabricius, 1798)

Abstract An evaluation of six dietary protein-to-energy (P/E) ratios was conducted to the early juvenile lobsters (Panulirus ornatus) by investigating the ratio effects on physiology, digestive enzyme activities, body composition, and amino acid profiles. Juvenile lobsters (0.25±0.01 g) were individually kept in aquaria and treated with six isoenergetic formulated diets of P/E ratios of 21.8, 22.5, 23.5, 24.6, 25.3 and 26.6 mg KJ−1. After 8 weeks of feeding experiment, the differentiation on dietary P/E ratios was found to have affected the specific growth rates, but not the survival, moult increment, moulting rate, moult interval and average daily moulting rate of juvenile lobsters. The dietary P/E ratio also influenced the protease, lipase, super oxidase dismutase activities, and body composition of juvenile lobster. The increase in dietary protein levels significantly affected the increase of the specific growth rate, while increased dietary lipid levels only affected the length increments. Both protein and lipid content were found in the whole body of the juveniles which reflected the treated dietary composition. Results indicated that a P/E ratio of 26.6 mg KJ−1 (55% dietary protein and 9% dietary lipids) can yield the maximum growth and digestive enzyme activities from among the studied diets.

Broodstock nutrition in Nile tilapia and its implications on reproductive efficiency

Broodstock nutrition is the most essential constituent of sustainable aquaculture production. Its impact on the reproductive performance and profitability of commercial aquaculture has been the subject of considerable research. The present paper reviews the literature available on the subject, examining the implication of Nile tilapia broodstock nutrition on parameters including maturation, fecundity, fertilization, embryo development, larval quality, and survival rate. The provision of a nutritive diet composed of essential macro- and micronutrients including proteins, lipids, carbohydrates, vitamins, minerals, and functional additives, such as prebiotics, enzymes, hormones, and probiotics, in different proportions is discussed. Special emphasis is given to literature dealing with the effects of dietary protein and lipid on vitellogenesis and ovarian maturation, fecundity, egg hatching rate, larval quality, and fry survival number. The impact of the feeding regime on reproductive performance is described.

Optimal dietary lipid levels alleviated adverse effects of high temperature on growth, lipid metabolism, antioxidant and immune responses in juvenile turbot (Scophthalmus maximus L.)

Fish physiological health is often negatively impacted by high-temperature environments and there are few studies on how dietary lipids affect fish growth and physiology when exposed to heat stress. The main objective of this research was to examine the impact of dietary lipid levels on growth and physiological status of juvenile turbot (Scophthalmus maximus L.) and determine if dietary lipid concentration could alleviate the possible adverse effects of heat stress. Five diets containing 6.81%, 9.35%, 12.03%, 14.74%, and 17.08% lipid, respectively, were formulated and fed to turbot (initial weight 5.13 ± 0.02 g) under high-temperature conditions (24.0–25.0 °C). Meanwhile, the diet with 12.03% lipid (considered by prior work to be an optimal dietary lipid level) was fed to turbot of the same size at normal temperature. Results suggested that, among the different dietary lipid levels under high-temperature conditions, fish fed the optimal lipid (12.03%) exhibited better growth compared to non-optimal lipid groups, as evidenced by higher weight gain and specific growth rate. Simultaneously, the optimal lipid diet may better maintain lipid homeostasis, as attested by lower liver and serum lipid, along with higher liver mRNA levels of lipolysis-related genes (pgc1α, lipin1, pparα, lpl and hl) and lower levels of synthesis-related genes (lxr, fas, scd1, pparγ, dgat1 and dgat2). Also, the optimal lipid diet might mitigate oxidative damage by improving antioxidant enzyme activity, decreasing malondialdehyde levels, and up-regulating oxidation-related genes (sod1, sod2, cat, gpx and ho-1). Furthermore, the optimal lipid may enhance fish immunity, as suggested by the decrease in serum glutamic-oxalacetic/pyruvic transaminase activities, down-regulation of pro-inflammatory genes and up-regulation of anti-inflammation genes. Correspondingly, the optimal lipid level suppressed MAPK signaling pathway via decreased phosphorylation levels of p38, JNK and ERK proteins in liver. In summary, the optimal dietary lipid level facilitated better growth and physiological status in turbot under thermal stress.

The interaction between lipid and vitamin D3 impacts lipid metabolism and innate immunity in Chinese mitten crabs Eriocheir sinensis

As a fat-soluble vitamin, vitamin D3 relies on fat to perform its biological function, affecting lipid metabolism and innate immunity. This study used different percentages of lipid and vitamin D3 diets to evaluate the synergistic effects on the growth, lipid metabolism and immunity of juvenile Eriocheir sinensis (5.83 ± 0.01 g) for 56 days, including low lipid (LL, 1.5%) and normal lipid (NL, 7.5%) and three levels of vitamin D3: low (LVD, 0 IU/kg), medium (MVD, 9000 IU/kg) and high (HVD, 27,000, IU/kg). The synergistic effect of lipid and vitamin D3 was not significant on growth but significant on ash content, total protein, hepatopancreas lipid content, hemolymph 1α,25-hydroxy vitamin D3 [1α,25(OH)2D3] content, hepatopancreas lipolysis and synthesis genes. Crabs fed normal lipid (7.5%) and medium vitamin D3 (9000 IU/kg) had the highest hepatopancreas index, hemolymph 1α,25(OH)2D3 content, antibacterial ability, immune-related genes and hepatopancreatic lipid synthesis genes expression, but down-regulated the lipolysis genes expression. In contrast, crabs fed diets with low lipid percentage (1.5%) had low growth performance, hemolymph 1α,25(OH)2D3, mRNA levels of lipid synthesis genes, antibacterial ability and immune-related gene expression. At the 1.5% lipid level, excessive or insufficient vitamin D3 supplementation led to the obstruction of ash and protein deposition, reduced growth and molting, aggravated the reduction in antioxidant capacity, hindered antimicrobial peptide gene expression and reduced innate immunity, and resulted in abnormal lipid accumulation and the risk of oxidative stress. This study suggests that diets' lipid and vitamin D3 percentage can enhance antioxidant capacity, lipid metabolism and innate immunity in E. sinensis. A low lipid diet can cause growth retardation, reduce antioxidant capacity and innate immunity, and enhance lipid metabolism disorder.

Physicochemical properties and sensory features of ripened, industrially prepared sausages, enriched with olive leaf extract to replace nitrite and nitrate

The use of nitrite and nitrate in meat products has been questioned due to the generation of N-nitroso compounds with carcinogenic effects. Thus, research has been focused on their replacement with several alternatives. This study is focused on evaluating the effects of a commercial olive leaf extract (OLE), marketed as dietary supplement, on protein and lipid oxidation, N-nitrosamine content and sensory properties of industrial sausages at the end of the ripening period. Five different formulations were prepared: F1 (OLE: 1000 mg/kg; NO2–NO3: 0 mg/kg), F2 (OLE: 1000 mg/kg; NO2–NO3: 75-75 mg/kg), F3 (OLE: 0 mg/kg; NO2–NO3: 0 mg/kg), F4 (OLE: 0 mg/kg; NO2–NO3: 75-75 mg/kg), F5 (OLE: 500 mg/kg; NO2–NO3: 35-35 mg/kg). The use of OLE in combination with a reduced dose of nitrite and nitrate (F5) significantly reduced the lipid and protein oxidation (p < 0.05) compared to the formulation with synthetic additives alone (F4). No differences were observed in terms of textural properties with the samples without the extract. The OLE did not affect the microbiological quality and enabled a significant reduction in the N-nitrosamines content. However, the addition of OLE decreased the intensity of red colour and determined the insurgence of a slight bitter taste in the sausages.

Tissue Distribution and Nutritional Regulation of Four Cholesterol Transport-Related Genes in Tiger Puffer (Takifugu rubripes)

This study characterized four cholesterol transport-related genes, namely, lcat, acat1, acat2, and mttp, in juvenile tiger puffer in terms of tissue distribution (eye, heart, brain, skin, liver, spleen, muscle, and intestine) and nutritional regulation. Three feeding trials were conducted: (i) using diets with different cholesterol levels (0.11%, 0.65%, 1.10%, 2.32%, and 4.59% of dry matter); (ii) using diets with different lipid levels (8.05%, 12.02%, and 16.36% of dry matter); and (iii) a 1-month starvation experiment with different sampling times (Days 1, 4, 9, 16, and 31). The lcat, acat1, and acat2 were the most abundantly expressed in the liver, while mttp was the most abundantly expressed in the intestine. The lcat had a medium expression level in the muscle and skin but the lowest expression level in the spleen and intestine. The acat1 and acat2 had similar tissue distribution patterns, except that acat2 had a lower expression level in the heart but a higher level in the intestine than acat1. The mttp had medium expression levels in the liver and spleen but had the lowest level in the eye and skin. Different dietary cholesterol levels did not significantly affect the expression of these cholesterol transport genes in the liver and intestine, except that higher cholesterol levels (1.10%–4.59%) significantly downregulated the acat2 expression in the liver. Dietary lipid levels also had a mild influence on the hepatic expression of these genes, except that the diet with 12.02% lipid resulted in significantly higher acat1 expression than the one with 16.36% lipid. The starvation time significantly affected the hepatic expression of these genes. Long-term starvation (16 and 31 days) generally upregulated the hepatic gene expression of lcat, acat1, and mttp but generally downregulated that of acat2. This study provided preliminary knowledge about the tissue distribution and nutritional regulation of cholesterol transport-related genes in marine teleost.

ACOD1 deficiency offers protection in a mouse model of diet-induced obesity by maintaining a healthy gut microbiota

Aconitate decarboxylase 1 (ACOD1) is the enzyme synthesizing itaconate, an immuno-regulatory metabolite tuning host-pathogen interactions. Such functions are achieved by affecting metabolic pathways regulating inflammation and microbe survival. However, at the whole-body level, metabolic roles of itaconate remain largely unresolved. By using multiomics-integrated approaches, here we show that ACOD1 responds to high-fat diet consumption in mice by promoting gut microbiota alterations supporting metabolic disease. Genetic disruption of itaconate biosynthesis protects mice against obesity, alterations in glucose homeostasis and liver metabolic dysfunctions by decreasing meta-inflammatory responses to dietary lipid overload. Mechanistically, fecal metagenomics and microbiota transplantation experiments demonstrate such effects are dependent on an amelioration of the intestinal ecosystem composition, skewed by high-fat diet feeding towards obesogenic phenotype. In particular, unbiased fecal microbiota profiling and axenic culture experiments point towards a primary role for itaconate in inhibiting growth of Bacteroidaceae and Bacteroides, family and genus of Bacteroidetes phylum, the major gut microbial taxon associated with metabolic health. Specularly to the effects imposed by Acod1 deficiency on fecal microbiota, oral itaconate consumption enhances diet-induced gut dysbiosis and associated obesogenic responses in mice. Unveiling an unrecognized role of itaconate, either endogenously produced or exogenously administered, in supporting microbiota alterations underlying diet-induced obesity in mice, our study points ACOD1 as a target against inflammatory consequences of overnutrition.

Prospective Monitoring of Small Intestinal Bacterial Overgrowth After Gastric Bypass: Clinical, Biological, and Gas Chromatographic Aspects.

Obesity is a predisposing factor for small intestinal bacterial overgrowth (SIBO). The aim of this study was to prospectively evaluate the prevalence of SIBO as well as its clinical, biological, and nutritional aspects before and up to 24months after a Roux-en-Y gastric bypass (RYGB) surgery. Fifty-one patients (mean BMI 46.9kg/m2, 66.7% women) requesting RYGB were included between 2016 and 2020. Each patient underwent a glucose breath test, a standardized interrogation on functional digestive signs, a dietary survey, a blood test, a fecalogram, and anthropometric data gathering. These investigations were carried out before surgery and at 1, 3, 6, 9, 12, 18, and 24months after RYGB. Before surgery, we found a prevalence of 17.6% of SIBO (95% CI = [8.9%; 31.4%]). After RYGB, at the end of 24months of follow-up, 89.5% of patients developed SIBO. Anal incontinence appeared to be very frequent after surgery, affecting 18.8% of our population 18months after surgery. We observed positive steatorrhea after surgery with an average of 11.1g of lipids/24h despite a significant limitation of dietary lipids (p = 0.0282). Our study corroborates data in the literature on the prevalence of SIBO in severe obesity patients. For the first time, we observed the sudden appearance of SIBO after RYGB, with a correlation between exhaled hydrogen on a breath test and lipid malabsorption on the fecalogram. As a result, these patients develop fatty diarrhea, with frequent fecal incontinence.

Phospholipids with two polyunsaturated fatty acyl tails promote ferroptosis

Phospholipids containing a single polyunsaturated fatty acyl tail (PL-PUFA1s) are considered the driving force behind ferroptosis, whereas phospholipids with diacyl-PUFA tails (PL-PUFA2s) have been rarely characterized. Dietary lipids modulate ferroptosis, but the mechanisms governing lipid metabolism and ferroptosis sensitivity are not well understood. Our research revealed a significant accumulation of diacyl-PUFA phosphatidylcholines (PC-PUFA2s) following fatty acid or phospholipid treatments, correlating with cancer cell sensitivity to ferroptosis. Depletion of PC-PUFA2s occurred in aging and Huntington's disease brain tissue, linking it to ferroptosis. Notably, PC-PUFA2s interacted with the mitochondrial electron transport chain, generating reactive oxygen species (ROS) for initiating lipid peroxidation. Mitochondria-targeted antioxidants protected cells from PC-PUFA2-induced mitochondrial ROS (mtROS), lipid peroxidation, and cell death. These findings reveal a critical role for PC-PUFA2s in controlling mitochondria homeostasis and ferroptosis in various contexts and explain the ferroptosis-modulating mechanisms of free fatty acids. PC-PUFA2s may serve as diagnostic and therapeutic targets for modulating ferroptosis.

Mitochondrial dysfunction in lipid processing and gastrointestinal disorders

Mitochondrial dysfunctions predominantly cause encephalomyopathies with muscle atrophy and neurodegeneration. However, their impact on other tissues, particularly the gastrointestinal tract, requires further investigation. In a recent report in Nature, Moschandrea et al. used mice deficient in the mitochondrial aminoacyl-tRNA synthetase DARS2 to investigate the role of enterocytic mitochondria in dietary lipid processing and transport. Their work sheds light on the development of gastrointestinal disorders as a result of mitochondrial dysfunction.

Combination of Gold Nanoparticles with Carnitine Attenuates Brain Damage in an Obesity Animal Model.

Obesity causes inflammation in the adipose tissue and can affect the central nervous system, leading to oxidative stress and mitochondrial dysfunction. Therefore, it becomes necessary to seek new therapeutic alternatives. Gold nanoparticles (GNPs) could take carnitine to the adipose tissue, thus increasing fatty acid oxidation, reducing inflammation, and, consequently, restoring brain homeostasis. The objective of this study was to investigate the effects of GNPs associated with carnitine on the neurochemical parameters of obesity-induced mice. Eighty male Swiss mice that received a normal lipid diet (control group) or a high-fat diet (obese group) for 10weeks were used. At the end of the sixth week, the groups were divided for daily treatment with saline, GNPs (70µg/kg), carnitine (500mg/kg), or GNPs associated with carnitine, respectively. Body weight was monitored weekly. At the end of the tenth week, the animals were euthanized and the mesenteric fat removed and weighed; the brain structures were separated for biochemical analysis. It was found that obesity caused oxidative damage and mitochondrial dysfunction in brain structures. Treatment with GNPs isolated reduced oxidative stress in the hippocampus. Carnitine isolated decreased the accumulation of mesenteric fat and oxidative stress in the hippocampus. The combination of treatments reduced the accumulation of mesenteric fat and mitochondrial dysfunction in the striatum. Therefore, these treatments in isolation, become a promising option for the treatment of obesity.

An insight into vitamin E and lipid nutrition of the plains-wanderer Pedionomus torquatus.

Vitamin E, as α-tocopherol, is an essential antioxidant protecting the body from free radicals. The vitamin E requirement of managed wildlife species is known to be greater than their wild counterparts, predominantly due to higher dietary lipid content and potentially stressful environments. The plains-wanderer (Pedionomus torquatus, Family Pedionomidae [monotypical]) is a critically endangered, superficially quail-like bird that is the focus of an ongoing captive breeding programme in Australia. It is estimated that plains-wanderers have a high vitamin E requirement (compared with domestic poultry species) to offset a high lipid diet and their naturally flighty temperament. This study therefore aims to gain a greater understanding of the nutritional status and vitamin E requirements of plains-wanderers in managed environments. Total lipid and α-tocopherol intake were quantified for 26 zoo-managed plains-wanderers over a series of diet intake trials in addition to measurement of plasma α-tocopherol and cholesterol concentrations. Plains-wanderers that consumed higher portions of dietary fat had significantly lower circulating α-tocopherol concentrations than birds that consumed lower total dietary fat (p < .001). Additionally, plasma cholesterol concentrations of managed plains-wanderers were found to be significantly greater than all other bird species reviewed, irrespective of Family or feeding type. We also present the first published data quantifying the nutritional makeup of stomach contents of a wild plains-wanderer for use as a potential guide for diet formulation. This study forms a vital foundational insight into the nutritional management of plains-wanderers, but further research is required to understand their dietary habits and cholesterol metabolism.

Intestinal mitochondria and dietary lipids.

Intestinal mitochondria and dietary lipids.

Epigenetic changes in pyloric caeca of Atlantic salmon fed diets containing increasing levels of lipids and choline

ABSTRACT An earlier study of ours investigating the effect of dietary lipid levels on the choline requirement of Atlantic salmon showed increasing severity of intestinal steatosis with increasing lipid levels. As choline is involved in epigenetic regulation by being the key methyl donor, pyloric caeca samples from the study were analysed for epigenetic effects of dietary lipid and choline levels. The diets varied in lipid levels between 16% and 28%, and choline levels between 1.9 and 2.3 g/kg. The diets were fed for 8 weeks to Atlantic salmon of 25 g of initial weight. Using reduced representation bisulfite sequencing (RRBS), this study revealed that increasing dietary lipid levels induced methylation differences in genes involved in membrane transport and signalling pathways, and in microRNAs important for the regulation of lipid homoeostasis. Increasing choline levels also affected genes involved in fatty acid biosynthesis and transport, lipolysis, and lipogenesis, as well as important immune genes. Our observations confirmed that choline is involved in epigenetic regulation in Atlantic salmon, as has been reported for higher vertebrates. This study showed the need for the inclusion of biomarkers of epigenetic processes in studies that must be conducted to define optimal choline levels in diets for Atlantic salmon.

12-week melatonin administration had no effect on diabetes risk markers and fat intake in overweight women night workers.

Interactions between circadian clocks and key mediators of chronic low-grade inflammation associated with fat consumption may be important in maintaining metabolic homeostasis and may pose a risk for the development of obesity-associated comorbidities, especially type 2 diabetes (T2DM). The aims of the present study were to evaluate the effects of melatonin administration on diabetes risk markers according to dietary lipid profile (pro-inflammatory versus anti-inflammatory) in excessive weight night workers, and to determine the effect of administration on fat consumption profile. A randomized, controlled, double-blind, crossover clinical trial involving 27 nursing professionals working permanent night shifts under a 12×36-hour system. The melatonin group (12 weeks) used synthetic melatonin (3 mg) only on days off and between shifts, while the placebo group (12 weeks) was instructed to take a placebo, also on days off and between shifts. For inflammatory characteristics, participants were divided into pro-inflammatory (saturated fats, trans fats and cholesterol) and anti-inflammatory (monounsaturated, polyunsaturated fats and EPA + DHA) groups according to fatty acid determinations. At baseline and at the end of each phase, blood glucose, insulin, glycosylated hemoglobin plasma concentrations were collected, and HOMA-IR was calculated. Melatonin administration for 12 weeks had no effect on T2DM risk markers according to dietary lipid profile (pro-inflammatory or anti-inflammatory potential) in excessive weight night workers. Among the limitations of the study include the fact that the low dose may have influenced the results expected in the hypothesis, and individual adaptations to night work were not evaluated. The insights discussed are important for future research investigating the influence of melatonin and fats considered anti- or pro-inflammatory on glucose and insulin homeostasis related to night work.

Intestinal Inflammation and Regeneration-Interdigitating Processes Controlled by Dietary Lipids in Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a disease of chronic inflammatory conditions of the intestinal tract due to disturbance of the inflammation and immune system. Symptoms of IBD include abdominal pain, diarrhea, bleeding, reduced weight, and fatigue. In IBD, the immune system attacks the intestinal tract's inner wall, causing chronic inflammation and tissue damage. In particular, interlukin-6 and interlukin-17 act on immune cells, including T cells and macrophages, to amplify the immune responses so that tissue damage and morphological changes occur. Of note, excessive calorie intake and obesity also affect the immune system due to inflammation caused by lipotoxicity and changes in lipids supply. Similarly, individuals with IBD have alterations in liver function after sustained high-fat diet feeding. In addition, excess dietary fat intake, along with alterations in primary and secondary bile acids in the colon, can affect the onset and progression of IBD because inflammatory cytokines contribute to insulin resistance; the factors include the release of inflammatory cytokines, oxidative stress, and changes in intestinal microflora, which may also contribute to disease progression. However, interfering with de novo fatty acid synthase by deleting the enzyme acetyl-CoA-carboxylase 1 in intestinal epithelial cells (IEC) leads to the deficiency of epithelial crypt structures and tissue regeneration, which seems to be due to Lgr5+ intestinal stem cell function. Thus, conflicting reports exist regarding high-fat diet effects on IBD animal models. This review will focus on the pathological basis of the link between dietary lipids intake and IBD and will cover the currently available pharmacological approaches.

Ishimozuku (Sphaerotrichia firma) lipids containing fucoxanthin suppress fatty liver and improve short chain fatty acid production in obese model mice

Ishimozuku (Sphaerotrichia firma) is one species of edible brown algae in Japan. The lipids contain rich of fucoxanthin and n-3 unsaturated fatty acids. This study analyzed dietary Ishimozuku lipid components and the effects on fatty liver and intestinal metabolite component production in obese model mice. Fatty acid composition and fucoxanthin contents of Ishimozuku lipids were analyzed by gas chromatography (GC) and high performance liquid chromatography (HPLC) analysis. Ishimozuku lipids contained fucoxanthin about 44.71 ± 0.02 mg/g. KK-Ay mice were fed with high-fat diet (Control) and a high-fat diet + 0.5% Ishimozuku lipid diet (Ishimozuku) for 4 weeks. Liver triglyceride contents and serum triglyceride concentrations were significantly lower in the Ishimozuku group than in the Control group. Results show that acetyl-CoA carboxylase (ACC) and stearoyl-CoA desaturase (SCD-1) mRNA expression were suppressed in the livers of Ishimozuku group mice. Furthermore, short chain fatty acid amounts in the cecal contents were greater in the Ishimozuku group mice. These results suggest that dietary Ishimozuku lipid components suppress liver lipid accumulation. Results also indicate Ishimozuku lipid components improve the balance of the intestinal microflora, which is disturbed by a high fat diet, and which promotes short chain fatty acid accumulation in the intestine. That accumulation is related to lipid and glucose metabolism.

Mapping the landscape of research on insulin resistance: a visualization analysis of randomized clinical trials

BackgroundInsulin resistance, a condition in which cells do not respond adequately to insulin, plays a crucial role in diabetes and related metabolic disorders. Randomized clinical trials (RCTs) explore interventions to manage insulin resistance, contributing to evidence-based medical progress. The current study aimed to analyze the global research landscape and trends in RCTs targeting insulin resistance.MethodsThis study used bibliometric analysis and data visualization to examine RCT publications on insulin resistance from 2003 to 2022. The Scopus database was used due to its comprehensive coverage. The search strategy involved combining terms related to insulin resistance with RCT-related terms. The search query was validated, and core bibliometric indicators were used to analyze publication growth, origin, productivity, quality, and citations.ResultsBetween 2003 and 2022, 1077 RCT-focused publications on insulin resistance were identified from a pool of 24,932 related articles. The growth followed two phases, with a significant increase after 2008. The USA (n = 308; 28.60%), Iran (n = 165; 15.32%), China (n = 110; 10.21%), and the UK (n = 92; 8.54%) were the main contributors. The active institutions included Tehran University of Medical Sciences (n = 38; 3.53%) and Harvard Medical School (n = 31; 2.88%). Prominent funding agencies include the National Institutes of Health (n = 88; 8.17%) and the National Institute of Diabetes and Digestive and Kidney Diseases (n = 86; 7.99%). The top journals included the American Journal of Clinical Nutrition (n = 44; 4.09%) and Diabetes Care (n = 35; 3.25%). Co-occurrence analysis revealed three clusters addressing “utilizing lipid panels as indicators of insulin resistance,” “analyzing the impact of diet composition and physical activity on insulin sensitivity among obese individuals,” and “exploring insulin resistance in cases of polycystic ovary syndrome.”ConclusionsThis comprehensive bibliometric analysis highlights the global research landscape and trends in RCTs targeting insulin resistance. Research on lipid panels, diet impact, and insulin resistance in patients with polycystic ovary syndrome will continue to be a hotspot. The findings offer valuable information on research priorities, international collaborations, and impactful publications. This study provides a foundation for future directorial investigations in this critical area of metabolic health.

Bile salt signaling and bile salt-based therapies in cardiometabolic disease.

Bile salts have an established role in the emulsification and intestinal absorption of dietary lipids, and their homeostasis is tightly controlled by various transporters and regulators in the enterohepatic circulation. Notably, emerging evidence points toward bile salts as major modulators of cardiometabolic disease (CMD), an umbrella disease of disorders affecting the heart and blood vessels that is caused by systemic metabolic diseases such as Type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD), the latter encompassing also metabolic dysfunction-associated steatohepatitis (MASH). The underlying mechanisms of protective effects of bile salts are their hormonal properties, enabling them to exert versatile metabolic effects by activating various bile salt-responsive signaling receptors with the nuclear farnesoid X receptor (FXR) and the Takeda G-protein-coupled receptor 5 (TGR5) as most extensively investigated. Activation of FXR and TGR5 is involved in the regulation of glucose, lipid and energy metabolism, and inflammation. Bile salt-based therapies directly targeting FXR and TGR5 signaling have been evaluated for their therapeutic potential in CMD. More recently, therapeutics targeting bile salt transporters thereby modulating bile salt localization, dynamics, and signaling, have been developed and evaluated in CMD. Here, we discuss the current knowledge on the contribution of bile salt signaling in the pathogenesis of CMD and the potential of bile salt-based therapies for the treatment of CMD.

Bioactives and their roles in bone metabolism of osteoarthritis: evidence and mechanisms on gut-bone axis.

Bioactives significantly modify and maintain human health. Available data suggest that Bioactives might play a beneficial role in chronic inflammatory diseases. Although promised, defining their mechanisms and opting to weigh their benefits and limitations is imperative. Detailed mechanisms by which critical Bioactives, including probiotics and prebiotics such as dietary lipids (DHA, EPA, alpha LA), vitamin D, polysaccharides (fructooligosaccharide), polyphenols (curcumin, resveratrol, and capsaicin) potentially modulate inflammation and bone metabolism is limited. Certain dietary bioactive significantly impact the gut microbiota, immune system, and pain response via the gut-immune-bone axis. This narrative review highlights a recent update on mechanistic evidence that bioactive is demonstrated demonstrated to reduce osteoarthritis pathophysiology.