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      A Review on the Protective Effects of Honey against Metabolic Syndrome

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          Abstract

          Metabolic syndrome (MetS) is a cluster of diseases comprising of obesity, diabetes mellitus, dyslipidemia, and hypertension. There are numerous pre-clinical as well as human studies reporting the protective effects of honey against MetS. Honey is a nutritional food low in glycemic index. Honey intake reduces blood sugar levels and prevents excessive weight gain. It also improves lipid metabolism by reducing total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) and increasing high-density lipoprotein (HDL), which leads to decreased risk of atherogenesis. In addition, honey enhances insulin sensitivity that further stabilizes blood glucose levels and protects the pancreas from overstimulation brought on by insulin resistance. Furthermore, antioxidative properties of honey help in reducing oxidative stress, which is one of the central mechanisms in MetS. Lastly, honey protects the vasculature from endothelial dysfunction and remodelling. Therefore, there is a strong potential for honey supplementation to be integrated into the management of MetS, both as preventive as well as adjunct therapeutic agents.

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

            Kimber L. Stanhope, Jean Schwarz, Nancy Keim … (2009)
            Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.
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              The return of metabolism: biochemistry and physiology of the pentose phosphate pathway

              Anna Stincone, Alessandro Prigione, Thorsten Cramer … (2014)
              The pentose phosphate pathway (PPP) is a fundamental component of cellular metabolism. The PPP is important to maintain carbon homoeostasis, to provide precursors for nucleotide and amino acid biosynthesis, to provide reducing molecules for anabolism, and to defeat oxidative stress. The PPP shares reactions with the Entner–Doudoroff pathway and Calvin cycle and divides into an oxidative and non-oxidative branch. The oxidative branch is highly active in most eukaryotes and converts glucose 6-phosphate into carbon dioxide, ribulose 5-phosphate and NADPH. The latter function is critical to maintain redox balance under stress situations, when cells proliferate rapidly, in ageing, and for the ‘Warburg effect’ of cancer cells. The non-oxidative branch instead is virtually ubiquitous, and metabolizes the glycolytic intermediates fructose 6-phosphate and glyceraldehyde 3-phosphate as well as sedoheptulose sugars, yielding ribose 5-phosphate for the synthesis of nucleic acids and sugar phosphate precursors for the synthesis of amino acids. Whereas the oxidative PPP is considered unidirectional, the non-oxidative branch can supply glycolysis with intermediates derived from ribose 5-phosphate and vice versa, depending on the biochemical demand. These functions require dynamic regulation of the PPP pathway that is achieved through hierarchical interactions between transcriptome, proteome and metabolome. Consequently, the biochemistry and regulation of this pathway, while still unresolved in many cases, are archetypal for the dynamics of the metabolic network of the cell. In this comprehensive article we review seminal work that led to the discovery and description of the pathway that date back now for 80 years, and address recent results about genetic and metabolic mechanisms that regulate its activity. These biochemical principles are discussed in the context of PPP deficiencies causing metabolic disease and the role of this pathway in biotechnology, bacterial and parasite infections, neurons, stem cell potency and cancer metabolism.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (iso-abbrev): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 02 August 2018
                Publication date Collection: August 2018
                Volume: 10
                Issue: 8
                Electronic Location Identifier: 1009
                Affiliations
                [1 ]Department of Anatomy, Faculty of Medicine, UKM Medical Centre, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia; nurzuliani@ 123456ums.edu.my
                [2 ]Department of Biomedical Sciences and Therapeutics, Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, 88400 Kota Kinabalu, Sabah, Malaysia; khairul.anwar@ 123456ums.edu.my
                [3 ]Department of Pharmacology, Faculty of Medicine, UKM Medical Centre, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia; chinkokyong@ 123456ppukm.ukm.edu.my
                [4 ]Department of Biochemistry, Faculty of Medicine, UKM Medical Centre, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia
                Author notes
                [* ]Correspondence: fairusahmad@ 123456ukm.edu.my ; Tel.: +60-3-9145-8632
                Author information
                https://orcid.org/0000-0001-6628-1552
                https://orcid.org/0000-0003-0766-6537
                Article
                Publisher ID: nutrients-10-01009
                DOI: 10.3390/nu10081009
                PMC ID: 6115915
                PubMed ID: 30072671
                SO-VID: 0612e9d9-eda2-4a17-8c47-a563f2f19fa8
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 07 July 2018
                Date accepted : 31 July 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: honey,diabetes mellitus,dyslipidemia,hypertension,obesity
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: honey, diabetes mellitus, dyslipidemia, hypertension, obesity

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