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According to the World Health Organisation (WHO), in 1980 the Global diabetes prevalence among adults was 4.7%, with approximately 108 million people affected. In 2014, this rose to 8.5%, with about 422 million people living with diabetes. (WHO Global Report on Diabetes (2016)). Looking at the WHO Diabetes Fact Sheet (updated 2023), the number of people living with diabetes has continued to rise. In 2021, WHO estimated 537 million adults (20–79 years) globally had diabetes (source: International Diabetes Federation data referenced by WHO).
Diabetes prevalence has been rising more rapidly in middle- and low-income countries. The disease is a major cause of blindness, kidney failure, heart attacks, stroke and lower limb amputation. We have even underestimated the diabetes rate: 347 million adult diabetics in 2008 already exceeded the 285 million estimated for 2010 (Shaw et al., 2009; Danaei et al.,2011).
These epidemics of obesity and diabetes contribute to the development of non-communicable diseases (NCDs), the foremost cause of death globally, leading to more deaths each year than all other diseases combined (WHO, 2012). Cardiovascular disease kills almost double the number of diabetics compared to the general population (Peters et al., 2014).
The complexity of these metabolic diseases makes proper treatment of the underlying causes very difficult. (Tiwari and Rao, 2002).
Metabolic Dysfunction Hyperinsulinemia (normoglycemia)Hypertension
Insulin resistance
Dyslipidemia (↑ Triglycerides, ↓ HDL cholesterol) Disease progression ➜ Type 2 Diabetes Hyper- to hypo-insulinemia
Hypertension
Insulin resistance
Hyperglycemia; Hypertriglyceridemia
Loss of pancreatic β-cell functional mass
Hypercholesterolemia (↓ HDL cholesterol)
Hyperglucagonemia
Endothelial dysfunction; Atherosclerotic plaque formation
Ectopic lipid deposition Obesity Adipocyte hypertrophy and hyperplasia
↑ Inflammation
Dyslipidemia (↑ Triglycerides, ↓ HDL cholesterol)
↑ Leptin resistance, ↓ Adiponectin
↓ Satiety signaling
↑ Hepatic lipodysfunction Figure 2. Schematic illustration of the close relationship between metabolic dysfunction, metabolic syndrome and development of type 2 diabetes. Common to all three are glucose intolerance, lipid dysfunction, inflammation and oxidative stress. [Compiled from Kahn et al. (2014); Kahn et al. (2006)]. Abbreviation: HDL, high density lipoprotein.
MECHANISM
The South African Medical Research Council has highlighted the potential of rooibos (Aspalathus linearis) in supporting metabolic health. Preclinical studies have shown that rooibos extracts, particularly those rich in Aspalathin, may help alleviate insulin resistance, enhance glucose uptake, and improve lipid metabolism. These effects have been reported in animal and in vitro models (Kawano et al., 2009; Muller et al., 2012; Kamakura et al., 2014; Mazibuko et al., 2014).
Aspalathin, a unique C-glucosyl dihydrochalcone flavonoid found in unfermented rooibos, has demonstrated antioxidant and anti-inflammatory properties. Research suggests that it can protect pancreatic β-cells against oxidative stress and inflammation, both of which are associated with poor diet, insulin resistance, and obesity (Son et al., 2012; Kamakura et al., 2014; Himpe et al., 2016).
A Japanese study reported that Aspalathin increased glucose uptake and insulin secretion in vitro and was effective in reducing hyperglycaemia and glucose intolerance in diabetic mouse models (Li et al., 2009). These findings suggest potential benefits for glycaemic control, although confirmation in human clinical trials is still limited.
Further research has indicated that rooibos and its bioactive compounds may provide cardioprotective effects in the context of diabetes, including reducing oxidative stress and improving cardiac function (Johnson et al., 2016). Additionally, studies have demonstrated that Aspalathus linearis exhibits potent antioxidant and anti-mutagenic properties, and may possess immune-modulating and chemo-preventive actions (McKay & Blumberg, 2007).
Adipocytes ↑ Apoptosis (via Fas and mitochondrial pathways)↓ Adipogenesis (↓ GPDH activity)
↓ Lipid peroxidation (brown adipose)
↓ Leptin, ↑ adiponectin
↓ Proliferation
↓ Intracellular TG
↑ Glucose uptake
(↑ GLUT4, PI3K) Liver ↓ Lipid accumulation (↓ FAS, HMGCoA reductase, ACAT)
↑ Glycogen (↑ GK, normalised G6Pase, ↓ PEPCK)
↑ SOD, CAT and GSH-dependent enzymes
↓ Hepatic lipase
↑ FA β-oxidation
↑ PPARα
↓ Glucose production
↓ TBARS, H₂O₂ Blood Plasma and Erythrocytes ↓ TBARS, H₂O₂ AMELIORATION OF HYPERGLYCAEMIA,
OXIDATIVE STRESS, OBESITY
AND DYSLIPIDAEMIA Gastro-Intestinal Tract Inhibition of
α-glucosidase
and α-amylase Skeletal Muscle ↑ Glucose uptake
(↑ GLUT4, PI3K, PPARγ) Pancreas ↑ PDX-1 and INS
↑ β-cell number
↓ Apoptosis
↑ Insulin
↑ Protection against gluco-lipotoxicity
↑ SOD, CAT and GSH-dependent enzymes Figure 2. Overview of the mechanisms of action of gallic, ferulic and chlorogenic acids on obesity and diabetes (as referenced in tables 7–9). (ACAT, acyl-CoA:cholesterol acyltransferase; CAT, catalase; FA, fatty acids; FAS, fatty acid synthase; GK, glucokinase; GLUT4, glucose transporter 4; G6Pase, glucose-6-phosphatase; GPDH, glycerol-3-phosphate dehydrogenase; GSH, glutathione; HMG-CoA reductase, 3-hydroxy-3-methylglutaryl coenzyme A reductase; INS, insulin gene; PDX-1, pancreatic and duodenal homeobox 1; PEPCK, phosphoenolpyruvate carboxykinase; PI3K, phosphatidylinositol-3-kinase; PPAR, peroxisomal proliferator-activated receptor; SOD, superoxide dismutase; TBARS, thiobarbituric acid reactive substances; TG, triglycerides).