Obesity, insulin resistance, hypertension and fatty liver, together termed metabolic syndrome, are key risk factors for cardiovascular disease. Chronic feeding of a diet high in saturated fats and simple sugars, such as fructose and glucose, induces these changes in rats. Naturally occurring compounds could be a cost-effective intervention to reverse these changes. Flavonoids are ubiquitous secondary plant metabolites; naringin gives the bitter taste to grapefruit. This study has evaluated the effect of naringin on diet-induced obesity and cardiovascular dysfunction in high carbohydrate, high fat-fed rats. These rats developed increased body weight, glucose intolerance, increased plasma lipid concentrations, hypertension, left ventricular hypertrophy and fibrosis, liver inflammation and steatosis with compromised mitochondrial respiratory chain activity. Dietary supplementation with naringin (approximately 100 mg/kg/day) improved glucose intolerance and liver mitochondrial dysfunction, lowered plasma lipid concentrations and improved the structure and function of the heart and liver without decreasing total body weight. Naringin normalised systolic blood pressure and improved vascular dysfunction and ventricular diastolic dysfunction in high carbohydrate, high fat-fed rats. These beneficial effects of naringin may be mediated by reduced inflammatory cell infiltration, reduced oxidative stress, lowered plasma lipid concentrations and improved liver mitochondrial function in rats.

Both black (B) and green (G) cardamom are used as flavours during food preparation. This study investigated the responses to B and G in a diet-induced rat model of human metabolic syndrome. Male Wistar rats were fed either a corn starch-rich diet (C) or a high-carbohydrate, high-fat diet with increased simple sugars along with saturated and trans fats (H) for 16 weeks. H rats showed signs of metabolic syndrome leading to visceral obesity with hypertension, glucose intolerance, cardiovascular remodelling and nonalcoholic fatty liver disease. Food was supplemented with 3% dried B or G for the final eight weeks only. The major volatile components were the closely related terpenes, 1,8-cineole in B and α-terpinyl acetate in G. HB (high-carbohydrate, high-fat + black cardamom) rats showed marked reversal of diet-induced changes, with decreased visceral adiposity, total body fat mass, systolic blood pressure and plasma triglycerides, and structure and function of the heart and liver. In contrast, HG (high-carbohydrate, high-fat + green cardamom) rats increased visceral adiposity and total body fat mass, and increased heart and liver damage, without consistent improvement in the signs of metabolic syndrome. These results suggest that black cardamom is more effective in reversing the signs of metabolic syndrome than green cardamom.

Saskatoon berry (Amelanchier alnifolia) is a potential functional food containing anthocyanins and flavonols, as well as ellagitannins and phenolic acids. We have determined the potential therapeutic effects of Saskatoon berry in diet-induced metabolic syndrome. Nine- to ten-week-old male Wistar rats were randomly assigned to four groups. Two groups were fed on control diets, either corn starch (C) or high-carbohydrate, high-fat diet (H) respectively, for 16 weeks. Two further groups were fed on C or H diet for 16 weeks with Saskatoon berry powder added to the diet for the final 8 weeks (CSSK, HSSK). After 16 weeks, H rats showed symptoms of metabolic syndrome, including increased body weight, visceral adiposity, systolic blood pressure, cardiac fibrosis, plasma concentrations of triglycerides and non-esterified fatty acids, and plasma activities of alanine transaminase and aspartate transaminase. Saskatoon berry intervention normalised body weight and adiposity, improved glucose tolerance, decreased systolic blood pressure, improved heart and liver structure and function with decreased infiltration of inflammatory cells, and decreased plasma total cholesterol. Further, Saskatoon berry normalised liver expression of hexokinase 1 and glycogen phosphorylase and increased glucose 6-phosphatase relative to H rats. These results suggest that Saskatoon berry regulates glycolysis, gluconeogenesis and glycogenesis to improve metabolic syndrome.

The pulp of the purple mangosteen, Garcinia mangostana, is a popular tropical fruit but the rind containing xanthones such as α-mangostin together with procyanidins and anthocyanidins is usually discarded as waste. However, this rind has been used in South-East Asia for diarrhoea, dysentery, skin infections and wounds. As xanthones have reported anti-inflammatory and antioxidant responses, this study has determined the bioactive compounds and evaluated the effects of G. mangostana rind on physiological, metabolic, liver and cardiovascular parameters in rats with diet-induced metabolic syndrome. Rats fed a diet with increased simple sugars and saturated fats developed obesity, hypertension, increased left ventricular stiffness, dyslipidaemia and fatty liver. Administration of G. mangostana rind as 5% of the food to rats with diet-induced metabolic syndrome gave a dose of 168 mg/kg/day α-mangostin, 355 mg/kg/day procyanidins, 3.9 mg/kg/day anthocyanins and 11.8 mg/kg/day hydroxycitric acid for 8 weeks which reduced body weight and attenuated physiological and metabolic changes in rats including decreased abdominal fat deposition, decreased abdominal circumference and whole-body fat mass, improved liver structure and function and improved cardiovascular parameters such as systolic blood pressure, left ventricular stiffness and endothelial function. These responses were associated with decreased infiltration of inflammatory cells, decreased deposition of collagen in both heart and liver and decreased mean adipocyte size in retroperitoneal adipose tissues. We conclude that, in rats with diet-induced metabolic syndrome, chronic intake of G. mangostana rind decreased infiltration of inflammatory cells which decreased physiological, metabolic, liver and cardiovascular symptoms.

Garcinia humilis is a fruit known as achachairú. It is native to South American countries such as Bolivia, Peru, and Brazil, but it is also cultivated as achacha in northern Australia. The aim of this study was to determine the phytochemicals in achacha rind and pulp and to investigate these components as potential treatments for the symptoms of metabolic syndrome. Both rind and pulp contain procyanidins and citric acid rather than hydroxycitric acid. Male Wistar rats (8⁻9 weeks old) were fed with either high-carbohydrate, high-fat, or corn starch diets for 16 weeks. Intervention groups were fed with either diet supplemented with 1.5% G. humilis rind powder or 2.0% G. humilis pulp for the last 8 weeks of the protocol. Rats fed a high-carbohydrate, high-fat diet exhibited hypertension, dyslipidemia, central obesity, impaired glucose tolerance, and non-alcoholic fatty liver disease. G. humilis rind decreased systolic blood pressure, diastolic stiffness, left ventricular inflammatory cell infiltration, and collagen deposition in high-carbohydrate, high-fat diet-fed rats. However, there was no change in glucose tolerance, body weight, or body composition. Therefore, G. humilis rind, usually a food by-product, but not the edible pulp, showed potential cardioprotection with minimal metabolic changes in a rat model of diet-induced metabolic syndrome.

The red seaweed, Kappaphycus alvarezii, was evaluated for its potential to prevent signs of metabolic syndrome through use as a whole food supplement. Major biochemical components of dried Kappaphycus are carrageenan (soluble fiber ~34.6%) and salt (predominantly potassium (K) 20%) with a low overall energy content for whole seaweed. Eight to nine week old male Wistar rats were randomly divided into three groups and fed for 8 weeks on a corn starch diet, a high-carbohydrate, high-fat (H) diet, alone or supplemented with a 5% (w/w) dried and milled Kappaphycus blended into the base diet. H-fed rats showed symptoms of metabolic syndrome including increased body weight, total fat mass, systolic blood pressure, left ventricular collagen deposition, plasma triglycerides, and plasma non-esterified fatty acids along with fatty liver. Relative to these obese rats, Kappaphycus-treated rats showed normalized body weight and adiposity, lower systolic blood pressure, improved heart and liver structure, and lower plasma lipids, even in presence of H diet. Kappaphycus modulated the balance between Firmicutes and Bacteroidetes in the gut, which could serve as the potential mechanism for improved metabolic variables; this was accompanied by no damage to the gut structure. Thus, whole Kappaphycus improved cardiovascular, liver, and metabolic parameters in obese rats.

Linseed is a dietary source of plant-based ω-3 fatty acids along with fiber as well as lignans including secoisolariciresinol diglucoside (SDG). We investigated the reversal of signs of metabolic syndrome following addition of whole linseed (5%), defatted linseed (3%), or SDG (0.03%) to either a high-carbohydrate, high-fat or corn starch diet for rats for the final eight weeks of a 16-week protocol. All interventions reduced plasma insulin, systolic blood pressure, inflammatory cell infiltration in heart, ventricular collagen deposition, and diastolic stiffness but had no effect on plasma total cholesterol, nonesterified fatty acids, or triglycerides. Whole linseed did not change the body weight or abdominal fat in obese rats while SDG and defatted linseed decreased abdominal fat and defatted linseed increased lean mass. Defatted linseed and SDG, but not whole linseed, improved heart and liver structure, decreased fat vacuoles in liver, and decreased plasma leptin concentrations. These results show that the individual components of linseed produce greater potential therapeutic responses in rats with metabolic syndrome than whole linseed. We suggest that the reduced responses indicate reduced oral bioavailability of the whole seeds compared to the components.