The Mechanism of Honey in Reversing Metabolic Syndrome

Abstract

Metabolic syndrome is a constellation of five risk factors comprising central obesity, hyperglycaemia, dyslipidaemia, and hypertension, which predispose a person to cardiometabolic diseases. Many studies reported the beneficial effects of honey in reversing metabolic syndrome through its antiobesity, hypoglycaemic, hypolipidaemic, and hypotensive actions. This review aims to provide an overview of the mechanism of honey in reversing metabolic syndrome. The therapeutic effects of honey largely depend on the antioxidant and anti-inflammatory properties of its polyphenol and flavonoid contents. Polyphenols, such as caffeic acid, p-coumaric acid, and gallic acid, are some of the phenolic acids known to have antiobesity and antihyperlipidaemic properties. They could inhibit the gene expression of sterol regulatory element-binding transcription factor 1 and its target lipogenic enzyme, fatty acid synthase (FAS). Meanwhile, caffeic acid and quercetin in honey are also known to reduce body weight and fat mass. In addition, fructooligosaccharides in honey are also known to alter lipid metabolism by reducing FAS activity. The fructose and phenolic acids might contribute to the hypoglycaemic properties of honey through the phosphatidylinositol 3-kinase/protein kinase B insulin signalling pathway. Honey can increase the expression of Akt and decrease the expression of nuclear factor-kappa B. Quercetin, a component of honey, can improve vasodilation by enhancing nitric oxide production via endothelial nitric oxide synthase and stimulate calcium-activated potassium channels. In conclusion, honey can be used as a functional food or adjuvant therapy to prevent and manage metabolic syndrome.

Caffeic Acid on Metabolic Syndrome: A Review

“…Eventually, hyperinsulinemia will occur as a negative feedback from the target cells, signaling inadequate insulin response, and, in turn, the pancreatic β-cells will produce more insulin. The prolonged inability to correct the state of insulin resistance will eventually give rise to hyperglycemia and type 2 diabetes [ 60 ].…”

“…Evidence concurred that 65–75% of the risk factor for primary hypertension is contributed by obesity and excess weight gain [ 82 ]. Besides, insulin resistance has also been linked to hypertension as insulin is able to cross the blood–brain barrier and subsequently activate the systemic nervous system, in addition to its ability to upregulate the angiotensin II (AT-II) receptor and reduce NO [ 60 ]. NO is one of the most important ROS in the cardiovascular system.…”

Preventive Impact of Long-Term Ingestion of Chestnut Honey on Glucose Disorders and Neurodegeneration in Obese Mice

“…In particular, dietary honey supplementation prevented the fasting hyperglycemia and the impairment of the glucose response during the glucose tolerance test, and it improved the plasma insulin concentration, insulin sensitivity and HOMA index, suggesting a preventive effect of the long-term honey ingestion in HFDinduced impairment of glucose homeostasis. On the other hand, honey hypoglycemic properties have been pointed out not only in diabetes rodent models but also in healthy subjects and diabetic patients [17,22,37,38]. In our experimental conditions, we did not observe any significant impact on weight gain or plasma lipid concentrations in HFD-H mice, ruling out an improvement of lipid metabolism as responsible for the observed effects on glucose metabolism.…”

“…The health-promoting characteristics are due to the presence of molecules with recognized antioxidants and anti-inflammatory properties [17]. Although honey is speculated to be a potential agent in preventing and reversing metabolic syndrome by reducing obesity, hyperglycemia, dyslipidemia and hypertension [18][19][20][21][22], the consequences of honey chronic ingestion on glucose homeostasis are still debated, and the impact on brain health conditions remains poorly known. Therefore, the present study was undertaken in order to evaluate the effects of regular honey intake on HFD-induced neurodegeneration in an animal model.…”

Neuronal nitric oxide synthases in the pathogenesis of metabolic syndrome

“…Так, при действии инсулина предварительная обработка миофибрилл с помощью Akti-2, ингибитора Akt2-киназы, снижала фосфорилирование nNOS по Ser1446, в то время как дорсоморфин, ингибитор AMФ-активируемой протеинкиназы, в этом случае был не эффективен [15]. Поскольку в условиях МС отмечается нарушение толерантности к глюкозе, а также ослабление инсулино-вого сигналинга в скелетных мышцах [76,77], это должно приводить к ослаблению стимулирующего влияния инсулина на nNOS, что неизбежно сопровождается нарушением в этих клетках и ткани в целом NO/цГМФ-зависимого сигналинга. В свою очередь, физические нагрузки, которые нормализуют энергетический обмен в клетках, восстанавливая активность AMФ-активируемой протеинкиназы [76,77], могут положительно влиять и на активность nNOS, и на зависимый от нее транспорт глюкозы, что требует дальнейших исследований [78,79,80].…”