The current study tested the hypothesis that supplementing a single HF breakfast with 3 g of cinnamon would delay GE of a high-fat solid meal utilizing the 13C octanoic acid breath test, and consequently reduce postprandial blood glucose and lipid concentrations.
Gastric Emptying, Metabolic Variables and Appetite
We were unable to induce significant changes in GE using 3 g of cinnamon. The test meal (65% of energy from fat) was mainly from sunflower oil, which contains approximately 70% linoleic acid (C18:2n-6, a PUFA ). Long-chain fatty acids have a potent inhibitory effect on GE rate [20, 32] and have also been shown to increase CCK and GLP-1 concentrations . We propose that cinnamon does not delay GE over and above the effects of the fat content of the meal. Furthermore, we found similar postprandial glycemic and lipemic responses under both conditions. However, it should be noted that we were unable to measure a hyperglycemic or hyperlipidemic state. Studies which employed the largest doses of cinnamon relative to carbohydrate in the test meal (carbohydrate/cinnamon ratio of 15 or lower [9, 13]) appear to have had the most potent effects on reducing postprandial glycemia . In spite of the current high ratio of 14, we did not achieve a significant blood glucose-lowering effect. This is possibly due to glucose absorption from the small intestine being affected by the fat content of a meal .
Recent data indicates that the addition of 3 g cinnamon to a low-fat rice pudding test meal had no significant effect on GE rate or postprandial glycemia in healthy individuals . However, cinnamon did significantly lower serum insulin levels and increase GLP-1 concentrations, a GI peptide which has been shown to increase glucose-dependent secretion of insulin, delay GE and reduce glucose absorption and postprandial glycemia [36, 37]. When added to the same test meal, 6 g cinnamon significantly delayed GE and reduced postprandial glycemia but the decrease in blood glucose concentration was more apparent than the delay in GE rate suggesting that GE cannot be the sole mechanism explaining lower blood glucose responses following cinnamon ingestion . Agreeing with the findings of others [13, 33, 34], we found that cinnamon did not influence appetite sensations or subsequent food intake, probably as a result of similar GE rates between conditions . Together with data presented in the current study, cinnamon is unlikely to be relevant in affecting the postprandial response to HF meals.
Diet and fatty acid intake
Assessment of previous day dietary intake indicated that a higher intake of C16:1, C20:1 and total n-3 was associated with a shorter GE Thalf of the HF meal supplemented with the wheat flour placebo. To our knowledge, this is the first observation of specific dietary fatty acids from preceding diet affecting GI transit in humans. A single meal, supplemented with n-3 PUFAs, was less capable of triggering GLP-1 and CCK compared to other fats, resulting in a more rapid GE of a HF breakfast  while others showed that n-3 PUFA fish oil reduced CCK release and gallbladder contraction without affecting GE . Both GLP-1 and CCK are putative mediators of the ileal brake, a feedback mechanism responsible for delaying transit and facilitating digestion, in response to lipids in the distal GI tract . Our current findings extend these observations to illustrate that even short-term intake of n-3 fatty acids is associated with faster GE rates, in a population who were not eating a HF diet. This means that mechanisms apart from acute release of GLP-1 and CCK, must mediate the effects of specific fatty acids on GI transit. Recently, a 3-day HF yoghurt supplementation, rich in C18:2n-6 accelerated the GE rate of a test meal rich in the same fatty acid . It is interesting to note that background intake of C18:2n-6, which was high in the test meal, did not show a strong association with GE of the meal. Our observations suggest that GE Thalf of a HF meal is not just specifically affected by a background intake of that specific fatty acid and that the process of adaptation to a HF diet may involve mechanisms other than desensitization to a specific fatty acid. It is likely that different adaptations are continuously taking place in the gut, in response to the balance of fatty acids in the diet. It is tempting to speculate about the potential mechanisms for fat sensing and adaptation following the recently sequenced GPR120 protein, expressed on intestinal cells, and demonstrated to be differentially sensitive to different fatty acids .
Vascular Function and antioxidant capacity
One of the principle findings of this study was that no changes were observed in relation to the measures of vascular function. Interestingly, there was a main effect for time indicating a decrease in SI which at face value appears paradoxical given the transient impairment in vessel function following the ingestion of a HF meal [44, 45]. This apparent contradiction might be explained by the fact the test meal we used may not have been of sufficient energy and, in particular, fat content to evoke a change in vessel function. In most of the related literature the postprandial TAG concentration associated with vascular dysfunction (~2.0 mmol/l; [17, 18, 44]) is double than that presently observed. Moreover, the HF meal in the current study contained 297 - 1742 kJ less energy (and 14 - 34 g less fat) than other similarly designed investigations [17, 45–47]. Such discrepancies in meal composition further highlight the need for a standardized, physiologically relevant HF meal  to be used in future corresponding studies, similar to the OGTT.
Due to its polyphenolic nature, cinnamon is thought to exhibit antioxidant properties [3, 49] which may be anti-atherogenic. It is proposed that the impairments in blood vessel function following the ingestion of HF loads are perpetrated via an oxidative stress mechanism that can increase the unwanted consumption of NO and favor the formation of further ROS, such as peroxynitrite (ONOO-) [17–19, 28, 44]. In the present study cinnamon ingestion had no apparent effect on indices of oxidative stress as a main effect for time was observed for LOOHs.
It has been documented that even high-normal fasting glucose levels can aggravate arterial stiffness  but when cinnamon was added to rats fed a high-fat high-fructose diet hepatic glycogen, hepatic insulin receptors and glut4 transporter in muscle tissue all increased . Despite no reported change in arterial stiffness using our physiologically relevant high-fat meal, the possibility therefore exists that cinnamon could modulate stiffness by affecting (hepatic) glycemic control and thus this relationship merits further scrutiny.
Emerging research postulates the existence of a diurnal variation in endothelial function . Fluctuations in the competitive balance between intrinsic local vasodilator function and sympathetic nervous system (SNS) α-adrenoreceptor-mediated vasoconstriction have recently been proposed as one potential mechanism to explain such findings . Given the conceptual relationship between endothelial function and arterial stiffness, and the observed main effect for a decrease in HR (as an indirect measure of SNS activity), it is tempting to speculate that this explanation may in some way account for the SI data in the current investigation. Conversely, this was tempered by the fact that no changes in RI were recorded.
This study may have been underpowered and therefore a small effect below the detection threshold of the study cannot be ruled out. Three grams of cinnamon was used as because it was shown to have a similar chronic effect on fasting serum glucose and lipid profiles as 6 g . However, recent evidence suggests a dose-dependent relationship for cinnamon consumed and the delay in GE [13, 35].