The main fruit sources of Cyanidins are Blackberries and Bilberries; approximately 80% of the Cyanidin content is in the form of Cyanidin-3-Glucoside (Cyanidin bound to glucose) and about 20% in the form of Cyanidin-3-Rutinoside (Cyanidin bound to the disaccharide rutinose). Trace amounts come from less abundant Cyanidin moieties (3,5-diglucose, 3-galactose).
Other dietary sources include chokeberries, boysenberries, elderberries, purple vegetables (such as carrots and yams), black raspberries, and Hibiscus sabdariffa extract. Basically, dark blue to purple colored plants. Interestingly, the darker than normal color in blood oranges relative to normal oranges is due to cyanidin compounds. Red cabbage (reddish-purple in nature) is also a source of novel cyanidin glycosides.
Although the cyanidin molecule does not change, it is found in a wide variety of differing glucosides; or bound to different sugars. Such as:
Cyanidin-3-Glucosides (Bound to Glucose)
Both the isolated cyanidin molecule as well as the glucoside (above bulleted compounds) may exert different effects.
Cyanidins share the typical anthocyanin backbone, but with a hydroxylation (addition of -OH) on one of its two possible sidechains (the R1 sidechain). The other is merely hydrogenated. If both side chains were hydroxylated, the compound would be a Delphinidin.
The form that is most well researched is Cyanidin-3-O-b-Glucoside, a form found occurring in foods and is sometimes found in the blood even with the glucose moiety still attached.
The stomach is a novel site for uptake of dietary cyanidins and cyanidins from food components. It allows for rapid delivery into the blood and avoids hepatic metabolism. The acidic environment of the stomach is also conducive to anthocyanin stability.
Uptake of Cyanidins bound to monosaccharides (like glucoside) are taken up fairly well, whereas those with larger sugar sidechains (such as Rutinoside) are hindered somewhat. Lower doses seem to have higher uptake percentages than higher dosages, implicating gastric digestion as a site for cost-efficacy supplementation and may be a reason that after ingestion of anthocyanins their intact glycosides can be found in the blood almost immediately.
Cyanidins are absorbed in the small intestine, like many anthocyanins, moderately well to poorly. Cyanidins had an uptake rate of 19.1% in one rat study and had an intestinal decay rate of 2.32 ± 0.67% to 22.4 ± 2.0% over 45 minutes. The most intestinally stable form of Cyanidins appears to be the 3-glucoside, although all cyanidins appear to be sensitive to the alkaline environment.
These rates may be much higher when paired with a Labrasol emulsifier, as one study to look at in vivo effects noted significance in a Labrasol + C3G group rather than a group without Labrasol. However, no studies have confirmed this increased rate of absorption beyond this.
One review looked at cyanidin bioavailability from various foods, and summarized the percentage of an oral dose (from various foods) of various cyanidin compounds that was absorbed and excreted in the urine was between 0.018-0.37%, with an average of less than a thousandth absorbed. Highest (measured) Cmax was 95-96nmol of cyanidin compounds, measured at an oral intake of 720mg. All mentioned studies collected urine for between 7 and 24 hours, and used varying glycosides of cyanidin, and would thus exclude longer pharmacokinetics.
When measured in the blood, cyanidins appear to exist primarily as metabolites of the liver. One study found that after ingestion of 721mg Cyanidin-3-Glucoside, that 32.5% of what was taken up was the parent compound, whereas 67.5% existed as metabolites, as a mixture of methylated conjugates (primarily) and sulphates and glucuronides. Oxidized metabolites of cyanidin have also been noted in serum.
It appears that the main pathway of metabolism for cyanidin compounds, after being cleaved from their glycosides, is either glucuronidation or methylation by P450 enzymes. One study noted that only two studies have found significant levels of sulphation end products, so this may not be a major metabolite in vivo. It appears that methyl end products are most prominent followed by glucuronides with sulphation end products coming in last.
Cyanidin that is bound to a disaccharide (like rutinose) or larger molecules appear to not be highly conjugated like those bound to monosaccharides. These compounds are taken up and excreted as their intact molecules.
Interestingly, despite the low amount of cyanidins present in the blood after ingestion it may be due to excessive conversion to protocatechuic acid. One study noted that 44% of an oral dose of Cyanidin-3-glucoside could be accounted for as protocatechuic acid, and that it was not able to be measured in the urine (but instead excreted fecally). In this study, 71mg of Cyanidin-3-Glucoside caused a Cmax of 492+/-62nmol/L for protocatechuic acid between 30-120 minutes after consumption, where serum values for Cyanidin-3-Glucoside itself were 1.9+/-0.6nmol/L. This degradation may be spontaneous rather than enzyme mediated.
Among bioflavonoids, cyanidins are fairly well taken up into the intestine's epithelial wall at around 20% of an oral dose. However, only a minimal amount (less than 2%) reaches the blood, with most being conjugated by P450; biological significance of these conjugates is not known. Unless measures are taken to increase bioavailability, or Cyanidins are otherwise superloaded (so 2% is a clinically significant amount), then oral supplementation may not yeild acute results.
Cyanidin supplementation may be a good source of protocatechuic acid though.
Like many polyphenols, C3G and related anthocyanins can beneficially affect adipocyte signalling properties, causing an increase in secreted adiponectin levels and a decrease in interleukin-6 and plasminogen activator inhibitor-1 activity. Promoting an anti-inflammatory overall effect.
Cyanidins are also able to promote phosphorylation and subsequent nuclear exclusion of FoxO1 (Forkhead Box Protein O1) during feeding, a gene which induces skeletogenesis and protein genesis in osteoblasts but hinders protein synthesis in myocytes via mTOR interference. Exclusion from the nucleus (interfering with transcripton) makes the effects of FoX01 less potent.
Although the Lipoprotein Lipase (LPL) enzyme is activated in muscle cells, it appears to be suppressed in visceral fat cells with Cyanidin-3-Glucoside administration, with no effect on subcutaneous. These effects were seen through AMPK phosphorylation, suggesting a different mechanism of action.
Uncoupling protein 2 (UCP2) was also induced in cells treated with C3G.
Paradoxically to the above actions, some actions of cyanidins are similar to insulin. Incubating cells with Cyanidins as Cyanidin-3-O-b-Glucoside has been shown to increase the activity of PPARy.
Increased GLUT4 translocation and glucose uptake was also seen in these cells.
The overall effect that the above mechanisms should result in (prevention of obesity from diet, alleviation of diabetic progression) has been noted in animals fed an obesogenic diet, with Cyanidins (as Cyanidin-3-Glucoside) at 2g/kg bodyweight; a large dose not able to be gained through normal human consumption.
Cyanidin, typically researched through Cyanidin-3-Glucosides, seem to be able to promote a state of anti-inflammation in fat cells that can potentially alleviate dysregulation in signalling that precedes disease states. Additionally, fat cells can uptake glucose easier via GLUT4 translocation. In vitro studies suggest great potential for Cyanidins as anti-diabetic compounds, and await replication in in vivo models.
Cyanidins appear to be potent AMPK activators, with downstream effects of increasing glucose and lipid uptake into myocytes
The normally deleterious effects of AMPK activation on muscle growth (in which higher AMPK is inversely related with muscle protein synthesis) are diminished via FOXo1 exclusion, a nuclear protein which AMPK must work through to hinder protein synthesis. Thus Cyanidins may prevent the expected inhibition of muscle protein synthesis themselves.
C3G can exert anti-diabetic effects via stimulation of the GLUT4 transporter activity in fat cells, and reducing retinol binding protein 4 (RBP4) expression. The reduction in expression of RBP4 is correlated with decreased levels of TNF-alpha in white adipocytes as well, which is related to an anti-inflammatory state. These anti-inflammatory effects, via inhibiting c-Jun NH2-terminal kinase activation, can possibly protect fat cells from damages associated with a pro-diabetic diet. Adding on to these effects, Cyanidin in adipocytes is related to increasing adiponectin secretion from the cultured adipocytes.
Cyanidins also reduces the amount of reactive oxygen species (ROS) produced inside the adipocyte, thus possessing anti-oxidant capabilities.
Cyanidin may also exert anti-diabetic effects via acting on PPARy.
The effects seen in muscle cells downstream of AMPK activation (increasing LPL activity, increased glucose uptake) can also be seen as anti-diabetic.
One study suggest that a dose of 143.5mg/kg bodyweight and a dose of 297.5mg/kg bodyweight 'Cyanidin-3-Glucoside equivalents' anthocyanins resulted in a decrease of blood glucose levels by 33% and 51% respectively when paired with a drug transport system known as Labrasol. These results were reported to rival that of the diabetic drug Metformin. This particular study used the two anthocyanins 'Malvidin-3-O-glucoside' and 'delphinidin-3-O-glucoside' as the C3G active components and found only the former to have active effects on reducing blood sugar, with the latter possibly interfering with the actions of malvidin-3-O-glucoside.
Cyanidins affect carcinogenesis in a number of ways. It can suppress the stimulation of pro-carcinogenic transcription factors which appear to be caused from inhibition of MAPK activity. 
It also possesses potent anti-oxidant abilities, particularily against OH- and O2 radicals.
Various animal models have shown anti-tumor effects with Cyanidin anthocyanins, delivered through Pomegranate Juice, Freeze dried berries, Berry extracts added to feed, and Cyanidins have directly been studied twice as components of feed.
Inositol Hexaphosphate has been shown to beneficially affect the bioavailability of blackcurrant anthocyanins when coingested, suggesting that the same mechanisms may apply to the Cyanidin subset.
A study noting synergisms in strawberries noted that, when isolated, Cyanidin had its anti-oxidative potential inhibited by Pelargonidin, which was alleviated with Quercetin being added. Quercetin itself was synergistic with Cyanidin, and Cyanidin's synergism with Quercetin is increased further with Ellagic Acid.