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1.
Cells ; 12(23)2023 11 25.
Article in English | MEDLINE | ID: mdl-38067134

ABSTRACT

The present study evaluated the ability of KlamExtra®, an Aphanizomenon flos aquae (AFA) extract, to counteract metabolic dysfunctions due to a high fat diet (HFD) or to accelerate their reversion induced by switching an HFD to a normocaloric diet in mice with diet-induced obesity. A group of HFD mice was fed with an HFD supplemented with AFA (HFD-AFA) and another one was fed with regular chow (standard diet-STD) alone or supplemented with AFA (STD-AFA). AFA was able to significantly reduce body weight, hypertriglyceridemia, liver fat accumulation and adipocyte size in HFD mice. AFA also reduced hyperglycaemia, insulinaemia, HOMA-IR and ameliorated the glucose tolerance and the insulin response of obese mice. Furthermore, in obese mice AFA normalised the gene and the protein expression of factors involved in lipid metabolism (FAS, PPAR-γ, SREBP-1c and FAT-P mRNA), inflammation (TNF-α and IL-6 mRNA, NFkB and IL-10 proteins) and oxidative stress (ROS levels and SOD activity). Interestingly, AFA accelerated the STD-induced reversion of glucose dysmetabolism, hepatic and VAT inflammation and oxidative stress. In conclusion, AFA supplementation prevents HFD-induced dysmetabolism and accelerates the STD-dependent recovery of glucose dysmetabolism by positively modulating oxidative stress, inflammation and the expression of the genes linked to lipid metabolism.


Subject(s)
Aphanizomenon , Animals , Mice , Aphanizomenon/metabolism , Mice, Obese , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Obesity/drug therapy , Obesity/metabolism , Diet, High-Fat/adverse effects , Inflammation/drug therapy , Glucose , RNA, Messenger/metabolism
2.
Int J Mol Sci ; 24(5)2023 Mar 01.
Article in English | MEDLINE | ID: mdl-36902167

ABSTRACT

Obesity and related metabolic dysfunctions are associated with neurodegenerative diseases, such as Alzheimer's disease. Aphanizomenon flos-aquae (AFA) is a cyanobacterium considered a suitable supplement for its nutritional profile and beneficial properties. The potential neuroprotective effect of an AFA extract, commercialized as KlamExtra®, including the two AFA extracts Klamin® and AphaMax®, in High-Fat Diet (HFD)-fed mice was explored. Three groups of mice were provided with a standard diet (Lean), HFD or HFD supplemented with AFA extract (HFD + AFA) for 28 weeks. Metabolic parameters, brain insulin resistance, expression of apoptosis biomarkers, modulation of astrocytes and microglia activation markers, and Aß deposition were analyzed and compared in the brains of different groups. AFA extract treatment attenuated HFD-induced neurodegeneration by reducing insulin resistance and loss of neurons. AFA supplementation improved the expression of synaptic proteins and reduced the HFD-induced astrocytes and microglia activation, and Aß plaques accumulation. Together, these outcomes indicate that regular intake of AFA extract could benefit the metabolic and neuronal dysfunction caused by HFD, decreasing neuroinflammation and promoting Aß plaques clearance.


Subject(s)
Aphanizomenon , Dietary Supplements , Neurodegenerative Diseases , Animals , Mice , Aphanizomenon/chemistry , Astrocytes/drug effects , Diet, High-Fat , Insulin Resistance , Microglia/drug effects , Neurodegenerative Diseases/prevention & control
3.
Nutrients ; 15(2)2023 Jan 16.
Article in English | MEDLINE | ID: mdl-36678333

ABSTRACT

Pre-obesity is a condition that predisposes to the risk of developing obesity, cardiovascular diseases (CVD), and diabetes. Our previous study demonstrated that a Cynara cardunculus (L.) based nutraceutical named Altilix® (Bionap, Italy), containing chlorogenic acid and luteolin extracts, was able to improve several hepatic and cardio-metabolic parameters. Given this background, we conducted a post-hoc analysis of the Altilix® study in order to analyze the supplement's effects in the subgroup of pre-obesity subjects on anthropometry (weight and waist circumference), glucose metabolism (HbA1C, HOMA-IR, and HOMA-ß), lipid profile (total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol), hepatic functionality (FLI, AST, ALT and AST/ALT), carotid-media thickness (CIMT) and endothelial function (FMD). Fifty subjects from the original study cohort (which consisted of 100 subjects) were chosen with BMI ≥ 25 and < 30 kg/m2. All subjects received the Altilix® supplement (150 mg/day) or placebo using a computer-based random allocation system. After six months of treatment Altilix® significantly reduced body weight, glycemic, and lipid parameters (total cholesterol, triglycerides, LDL-cholesterol) and improved hepatic functionality, CIMT, and FMD. In conclusion, these results confirm that Altilix® supplementation has a significant effect on cardiometabolic parameters not only in obese subjects but also in pre-obesity subjects.


Subject(s)
Cardiovascular Diseases , Chlorogenic Acid , Humans , Luteolin , Obesity , Dietary Supplements , Triglycerides , Cholesterol , Cardiovascular Diseases/prevention & control , Double-Blind Method
4.
Nutrients ; 14(4)2022 Feb 11.
Article in English | MEDLINE | ID: mdl-35215406

ABSTRACT

The purpose of the present study was to evaluate the impact of long-term honey ingestion on metabolic disorders and neurodegeneration in mice fed a high-fat diet (HFD). Three groups of mice were fed with a standard diet (STD), HFD or HFD supplemented with honey (HFD-H) for 16 weeks. Biochemical, histological, Western blotting, RT-PCR and Profiler PCR array were performed to assess metabolic parameters, peripheral and central insulin resistance and neurodegeneration. Daily honey intake prevented the HFD-induced glucose dysmetabolism. In fact, it reduced plasma fasting glucose, insulin and leptin concentrations and increased adiponectin levels. It improved glucose tolerance, insulin sensitivity and HOMA index without affecting plasma lipid concentration. HFD mice showed a significantly higher number of apoptotic nuclei in the superficial and deep cerebral cortex, upregulation of Fas-L, Bim and P27 (neuronal pro-apoptotic markers) and downregulation of Bcl-2 and BDNF (anti-apoptotic factors) in comparison with STD- and HFD-H mice, providing evidence for honey neuroprotective effects. PCR-array analysis showed that long-term honey intake increased the expression of genes involved in insulin sensitivity and decreased genes involved in neuroinflammation or lipogenesis, suggesting improvement of central insulin resistance. The expressions of p-AKT and p-GSK3 in HFD-H mice, which were decreased and increased, respectively, in HFD mouse brain, index of central insulin resistance, were similar to STD animals supporting the ability of regular honey intake to protect brain neurons from insulin resistance. In conclusion, the present results provide evidence for the beneficial preventative impact of regular honey ingestion on neuronal damage caused by HFD.


Subject(s)
Honey , Insulin Resistance , Animals , Diet, High-Fat/adverse effects , Eating , Glucose , Glycogen Synthase Kinase 3 , Insulin Resistance/physiology , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity/metabolism
5.
Nutrients ; 13(10)2021 Sep 28.
Article in English | MEDLINE | ID: mdl-34684446

ABSTRACT

The blue-green algae Aphanizomenon flos aquae (AFA), rich in beneficial nutrients, exerts various beneficial effects, acting in different organs including the gut. Klamin® is an AFA extract particularly rich in ß-PEA, a trace-amine considered a neuromodulator in the central nervous system. To date, it is not clear if ß-PEA exerts a role in the enteric nervous system. The aims of the present study were to investigate the effects induced by Klamin® on the human distal colon mechanical activity, to analyze the mechanism of action, and to verify a ß-PEA involvement. The organ bath technique, RT-PCR, and immunohistochemistry (IHC) were used. Klamin® reduced, in a concentration-dependent manner, the amplitude of the spontaneous contractions. EPPTB, a trace-amine receptor (TAAR1) antagonist, significantly antagonized the inhibitory effects of both Klamin® and exogenous ß-PEA, suggesting a trace-amine involvement in the Klamin® effects. Accordingly, AphaMax®, an AFA extract containing lesser amount of ß-PEA, failed to modify colon contractility. Moreover, the Klamin® effects were abolished by tetrodotoxin, a neural blocker, but not by L-NAME, a nitric oxide-synthase inhibitor. On the contrary methysergide, a serotonin receptor antagonist, significantly antagonized the Klamin® effects, as well as the contractility reduction induced by 5-HT. The RT-PCR analysis revealed TAAR1 gene expression in the colon and the IHC experiments showed that 5-HT-positive neurons are co-expressed with TAAR1 positive neurons. In conclusion, the results of this study suggest that Klamin® exerts spasmolytic effects in human colon contractility through ß-PEA, that, by activating neural TAAR1, induce serotonin release from serotoninergic neurons of the myenteric plexus.


Subject(s)
Aphanizomenon/chemistry , Biological Products/pharmacology , Colon/drug effects , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Parasympatholytics/pharmacology , Aged , Aged, 80 and over , Biological Products/chemistry , Biomarkers , Colon/metabolism , Dietary Supplements , Dose-Response Relationship, Drug , Female , Gene Expression , Humans , Immunohistochemistry , Male , Middle Aged , Parasympatholytics/chemistry , Peristalsis/drug effects
6.
J Nutr Biochem ; 82: 108401, 2020 08.
Article in English | MEDLINE | ID: mdl-32454412

ABSTRACT

Honey is a natural product, containing flavonoids and phenolic acids, appreciated for its therapeutic abilities since ancient times. Although the bioactive potential is linked to the composition, that is variable depending on mainly the botanical origin, honey has antioxidant and anti-inflammatory properties. Therefore, honey, administered alone or in combination with conventional therapy, might result useful in the management of chronic diseases that are commonly associated with oxidative stress and inflammation state. Obesity is a metabolic disorder characterized by visceral adiposity. The adipose tissue becomes hypertrophic and undergoes hyperplasia, resulting in a hypoxic environment, oxidative stress and production of pro-inflammatory mediators that can be responsible for other disorders, such as metabolic syndrome and neurodegeneration. Experimental evidence from animals have shown that honey improves glycemic control and lipid profile with consequent protection from endothelial dysfunction and neurodegeneration. The purpose of the present review is to summarize the current literature concerning the beneficial effects of honey in the management of the obesity-related dysfunctions, including neurodegeneration. Based on the key constituents of honey, the paper also highlights polyphenols to be potentially responsible for the health benefits of honey. Further well-designed and controlled studies are necessary to validate these benefits in humans.


Subject(s)
Antioxidants/therapeutic use , Honey , Obesity/diet therapy , Animals , Anti-Inflammatory Agents/therapeutic use , Diabetes Mellitus, Type 2/diet therapy , Flavonoids/chemistry , Glycemic Control/methods , Health Status , Humans , Hydroxybenzoates/chemistry , Hyperplasia/diet therapy , Hypertension/diet therapy , Inflammation/diet therapy , Insulin Resistance , Metabolic Syndrome/diet therapy , Neurodegenerative Diseases/diet therapy , Oxidative Stress/drug effects , Polyphenols/chemistry , Polyphenols/therapeutic use
7.
Nutrients ; 10(12)2018 Dec 01.
Article in English | MEDLINE | ID: mdl-30513740

ABSTRACT

Pistachios contain beneficial substances such as unsaturated fatty acids, phytosterols, and polyphenols. In the present study, we investigated if pistachio consumption is able to prevent or to revert hyperglycemia, dyslipidemia, hepatic steatosis, and adipose tissue morphological alterations caused by high fat diet (HFD) in the mouse. Moreover, the impact of pistachio intake on the mRNA expression of peroxisome proliferator-activated receptor γ (PPAR-γ), fatty acid transport proteins (FAT-P), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD1), and sterol regulatory element-binding transcription factor-1c (SREBP-1c) in liver and adipose tissue was also analyzed. No change in body weight, food intake, and hyperglycemia was observed between mice consuming pistachios (HFD-P) and HFD mice. Pistachio intake was able to prevent but not to reverse HFD-induced hypertriglyceridemia. Cholesterol plasma levels, steatosis grading, body fat mass, and adipocyte size were significantly lower in HFD-P group compared to HFD in both prevention and reversal protocol. Pistachio-diet was able to prevent HFD-induced overexpression of PPAR-γ, FAS, and SCD1 in the liver and SREBP-1c, PPAR-γ, and FAT-P in adipose tissue. Similarly, HFD-P significantly ameliorated the expression levels of FAT-P and SCD1 in the liver and SREBP-1c, FAS, and SCD1 in adipose tissue of obese mice. The present study shows that pistachio consumption is able to prevent and to ameliorate obesity-related dysfunctions by positively modulating the expression of genes linked to lipid metabolism.


Subject(s)
Diet, High-Fat/adverse effects , Dyslipidemias/drug therapy , Lipid Metabolism/drug effects , Nuts , Obesity/metabolism , Pistacia/chemistry , Plant Extracts/pharmacology , Adipose Tissue/cytology , Adipose Tissue/metabolism , Animals , Cholesterol/blood , Diet , Dyslipidemias/etiology , Dyslipidemias/metabolism , Fatty Acid Synthases/metabolism , Fatty Liver/metabolism , Fatty Liver/prevention & control , Hypertriglyceridemia/metabolism , Hypertriglyceridemia/prevention & control , Lipid Metabolism/genetics , Liver/drug effects , Liver/metabolism , Male , Mice, Inbred C57BL , Mice, Obese , Obesity/drug therapy , PPAR gamma/metabolism , Phytosterols/pharmacology , Phytosterols/therapeutic use , Plant Extracts/therapeutic use , Polyphenols/pharmacology , Polyphenols/therapeutic use , RNA, Messenger/metabolism , Stearoyl-CoA Desaturase/metabolism , Sterol Regulatory Element Binding Protein 1/metabolism
8.
Nutrients ; 10(9)2018 Aug 21.
Article in English | MEDLINE | ID: mdl-30134549

ABSTRACT

Obesity and metabolic disorders can be risk factors for the onset and development of neurodegenerative diseases. The aim of the present study was to investigate the protective effects of a natural dietary supplement (NDS), containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin, on dysmetabolism and neurodegeneration in the brains of high fat diet (HFD)-fed mice. Decrease in the expression of FACL-4, CerS-1, CerS-4, cholesterol concentration and increase in the insulin receptor expression and insulin signaling activation, were found in brains of NDS-treated HFD brains in comparison with HFD untreated-mice, suggesting that NDS is able to prevent brain lipid accumulation and central insulin resistance. In the brains of NDS-treated HFD mice, the levels of RNS, ROS and lipid peroxidation, the expression of p-ERK, H-Oxy, i-NOS, HSP60, NF-kB, GFAP, IL-1ß, IL-6 and CD4 positive cell infiltration were lower than in untreated HFD mice, suggesting antioxidant and anti-inflammatory effects of NDS. The decreased expression of p-ERK and GFAP in NDS-treated HFD mice was confirmed by immunofluorescence. Lastly, a lower number of apoptotic nuclei was found in cortical sections of NDS-treated HFD mice. The present data indicate that NDS exerts neuroprotective effects in HFD mice by reducing brain fat accumulation, oxidative stress and inflammation and improving brain insulin resistance.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Antioxidants/pharmacology , Brain/drug effects , Diet, High-Fat , Dietary Supplements , Nerve Degeneration , Neurodegenerative Diseases/prevention & control , Animals , Apoptosis/drug effects , Brain/metabolism , Brain/pathology , Disease Models, Animal , Inflammation Mediators/metabolism , Insulin/metabolism , Insulin Resistance , Lipid Metabolism/drug effects , Lipid Peroxidation/drug effects , Male , Mice, Inbred C57BL , Neurodegenerative Diseases/metabolism , Neurodegenerative Diseases/pathology , Oxidative Stress/drug effects , Signal Transduction/drug effects
9.
Nutrients ; 9(5)2017 May 13.
Article in English | MEDLINE | ID: mdl-28505074

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular diseases. NAFDL is associated with atherogenic dyslipidemia, inflammation and renin-angiotensin system (RAS) imbalance, which in turn lead to atherosclerotic lesions. In the present study, the impact of a natural dietary supplement (NDS) containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin on NAFLD and atherosclerosis was evaluated, and the mechanism of action was examined. C57BL/6 mice were fed an HFD for 16 weeks; half of the mice were simultaneously treated with a daily oral administration (os) of the NDS. NAFLD and atherogenic lesions in aorta and carotid artery (histological analysis), hepatic expression of genes involved in the NAFLD (PCR array), hepatic angiotensinogen (AGT) and AT1R mRNA expression (real-time PCR) and plasma angiotensin (ANG)-II levels (ELISA) were evaluated. In the NDS group, steatosis, aortic lesions or carotid artery thickening was not observed. PCR array showed upregulation of some genes involved in lipid metabolism and anti-inflammatory activity (Cpt2, Ifng) and downregulation of some genes involved in pro-inflammatory response and in free fatty acid up-take (Fabp5, Socs3). Hepatic AGT, AT1R mRNA and ANG II plasma levels were significantly lower with respect to the untreated-group. Furthermore, NDS inhibited the dyslipidemia observed in the untreated animals. Altogether, these results suggest that NDS prevents NAFLD and atherogenesis by modulating the expression of different genes involved in NAFLD and avoiding RAS imbalance.


Subject(s)
Atherosclerosis/prevention & control , Dietary Supplements , Non-alcoholic Fatty Liver Disease/prevention & control , Administration, Oral , Angiotensin II/blood , Angiotensin II/genetics , Angiotensinogen/genetics , Angiotensinogen/metabolism , Animals , Chlorogenic Acid/pharmacology , Commiphora , Curcumin/pharmacology , Diet, High-Fat , Fatty Acid-Binding Proteins/blood , Fatty Acid-Binding Proteins/genetics , Gene Expression Regulation , Inulin/pharmacology , Lipid Metabolism/drug effects , Male , Mice , Mice, Inbred C57BL , Neoplasm Proteins/blood , Neoplasm Proteins/genetics , Plant Extracts/pharmacology , Plant Gums/pharmacology , RNA, Messenger/genetics , RNA, Messenger/metabolism , Silymarin/pharmacology , Suppressor of Cytokine Signaling 3 Protein/genetics , Suppressor of Cytokine Signaling 3 Protein/metabolism
10.
Endocrine ; 54(3): 648-656, 2016 Dec.
Article in English | MEDLINE | ID: mdl-26832341

ABSTRACT

Previous studies suggested that endogenous glucagon-like peptide 2 (GLP-2) is dispensable for the regulation of glucose homeostasis under normal conditions, while it can play a beneficial role in obesity conditions. The purpose of the present study was to investigate whether chronic treatment with Gly2-GLP-2, a stable analogue of GLP-2, can have an impact on glycaemic and lipid control in mice fed a high-fat diet (HFD), an animal model of human obesity and insulin resistance. HFD mice were treated once a day with Gly2-GLP-2 for 4 weeks. Body weight, food intake, fasting glucose, intraperitoneal glucose tolerance, insulin-induced glucose clearance, glucose-stimulated insulin secretion, ß-cell mass, plasma lipid metabolic profile, and lipid deposition in the liver were examined. In untreated HFD mice, fasting glucose levels, glucose tolerance, glucose-stimulated plasma insulin and sensibility to exogenous insulin were deteriorating with time and ß-cell mass increased. In Gly2-GLP-2-treated mice, we found significant increase in glucose tolerance and exogenous insulin sensitivity, reduction in glucose-stimulated plasma insulin and in the increase in ß-cell mass in comparison with pair-aged HFD untreated animals. The chronic treatment with the peptide was not associated with remarkable improvements of dyslipidemia and it did not prevent liver fat accumulation and the presence of microvesicular steatosis. In conclusion, the results of the present study suggest, for the first time, that Gly2-GLP-2 may produce glucose metabolic benefits in mice with diet-induced obesity. The mechanisms underlying the beneficial impact of GLP-2 on glucose metabolism remain to be established.


Subject(s)
Glucagon-Like Peptide 2/agonists , Glucose Metabolism Disorders/drug therapy , Peptides/therapeutic use , Animals , Diet, High-Fat , Drug Evaluation, Preclinical , Lipids/blood , Liver/drug effects , Male , Mice, Inbred C57BL , Pancreas/drug effects , Peptides/pharmacology , Random Allocation
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