scholarly journals The acute effect of baobab fruit on cognitive performance, cerebral blood flow and blood glucose levels.

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Sarah Docherty ◽  
Crystal Haskell-Ramsay

AbstractBaobab fruit contains high levels of phenolic compounds and vitamin C. Previous work has associated these phenolic compounds and vitamin C with a range of health benefits including improvements in cerebral blood flow and cognition. In vivo, it has been demonstrated that consumption of baobab fruit can reduce the glycaemic response, which may provide a mechanism for cognitive benefits as other research has shown that variations in blood glucose levels can modulate cognitive performance. Preliminary work found that consumption of 15 g baobab fruit extract significantly improved reaction time but increased number of errors on an executive function task. Taken together it would suggest baobab fruit has the potential to improve cognitive performance that could be attributed to changes in cerebral blood flow and blood glucose levels.The current study aimed to determine the effect of baobab fruit on cognitive performance, cerebral blood flow and blood glucose levels in a healthy young sample.This randomised, placebo-controlled, double-blind, counterbalanced-crossover study assessed the effect of 10 g baobab fruit powder or sugar matched control in 24 healthy participants (17 female, 7 male, mean age = 22.91 SD = 3.37). All participants completed the cognitive assessments, a subset of 14 completed the cerebral blood flow and blood glucose assessments (mean age = 23.21, SD = 2.46). Participants completed baseline tasks before consuming a drink containing either 10 g baobab fruit powder or placebo, there was then a 45-minute absorption period before participants completed cognitive tasks again. Seven days after participants returned and completed the same procedure but consumed the opposite drink. In the 14 participant subset, cerebral blood flow was measured throughout using Near Infrared Spectroscopy (NIRS) and blood glucose was measured before testing, after absorption period and upon completion of post doseUsing the MIXED procedure in SPSS, results showed that after consumption of baobab there was improved accuracy on a sustained attention task and fewer errors on the last repetition of a serial subtraction task. Baobab consumption led to increased blood glucose levels but there was no significant effect on cerebral blood flow.Results show that, in this sample, 10 g baobab fruit can improve certain aspects of cognitive performance and increase circulating blood glucose levels, which may explain these improvements. However, there was no significant effect on any cerebral blood flow measures. Future work may wish to explore further glucoregulation activity (in particular insulin response) after baobab consumption as a potential underlying mechanism.

PEDIATRICS ◽  
1990 ◽  
Vol 85 (2) ◽  
pp. 172-176 ◽  
Author(s):  
O. Pryds ◽  
N. J. Christensen ◽  
B. Friis-Hansen

Cerebral blood flow, plasma epinephrine, and plasma norepinephrine were measured in 25 spontaneously breathing, preterm neonates (mean gestational age 30.4 weeks) 2 hours after birth, during a routine screening for low blood glucose levels. Increased cerebral blood flow and plasma epinephrine values were observed when blood glucose levels were low, whereas plasma norepinephrine was constant throughout the blood glucose range. Hypoglycemia (defined as blood glucose concentration <30 mg/dL) was found in 13 neonates who were treated with intravenous glucose and milk enterally. Blood glucose levels were normal in the remaining 12 control neonates who received milk by a gastric line. Approximately 30 minutes after treatment with intravenous glucose and/or milk, cerebral blood flow had decreased by a mean of 11.3% in the 13 hypoglycemic neonates but was still 37.5% higher than cerebral blood flow in the control neonates despite normalization of plasma epinephrine concentration. Mean arterial blood pressure and blood gas values were identical between groups throughout the investigation. It is suggested that a normal coupling between cerebral metabolic demands and flow is present in very preterm neonates and that epinephrine may play a role in the cerebral hyperperfusion. Although none of the neonates had clinical signs of hypoglycemia, the data suggest that counterregulatory mechanisms are invoked when blood glucose values are <30 to 45 mg/dL.


1999 ◽  
Vol 19 (3) ◽  
pp. 288-297 ◽  
Author(s):  
Lars Gisselsson ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö

The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF.


Author(s):  
VIJAYAKRISHNA P ◽  
USHASREE TS ◽  
INDIRA K ◽  
AVULA NAVEEN ◽  
SHIRISHA S

Objectives: Diabetes mellitus (DM) is a spectrum of common metabolic disorders, arising from a variety of pathogenic mechanisms resulting in hyperglycemia that causes chronic micro- and macro-vascular complications. Vitamin C is structurally similar to glucose and can replace it in many chemical reactions and thus is effective in the prevention of non-enzymatic glycosylation of proteins. Hence, the present study taken up to see the effect of supplementation of Vitamin C on blood glucose and glycosylated hemoglobin (HbA1c) along with metformin in experimentally-induced diabetic rabbits. Methods: Twenty-four adult New Zealand white rabbits (1.5–2.5 kg) were divided into four groups, each containing six rabbits. Group 1: Normal control (distilled water); Group 2: Metformin (23.33 mg/kg) is given orally; Group 3: Metformin (23.33 mg/kg) plus Vitamin C 250 mg are given orally; and Group 4: Metformin (23.33 mg/kg) plus Vitamin C 500 mg are given orally. Animals were treated for 30 days. The blood samples were collected on days 0 and 30 from the marginal ear vein of rabbits for the estimation of blood glucose and HbA1c levels. Results: Statistically analyzed by ANOVA test followed by post hoc Tukey’s test using GraphPad Prism software. Results shown that Vitamin C 500 mg oral supplementation with metformin had very highly significantly reduced HbA1c levels by 40.12% (p = 0.0001***) and blood glucose levels by 49.12% (p = 0.0003***), whereas Vitamin C 250 mg oral supplementation with metformin also significantly reduced HbA1c levels by 25.49% (p = 0.0001***) and blood glucose levels by 42.95% (p = 0.0026**) when compared to metformin alone, which reduced HbA1c levels by 22% (p = 0.0001***) and blood glucose levels by 39.58% (p = 0.0001***). Conclusion: Oral supplementation of Vitamin C 500 mg/250 mg to the metformin was superior in reducing HbA1c levels and blood glucose levels compared to metformin alone in rabbits. Hence, Vitamin C oral supplementation may be helpful in lowering blood glucose levels and HbA1c levels and improving glycemic control in Type 2 DM.


1993 ◽  
Vol 264 (4) ◽  
pp. H1069-H1075 ◽  
Author(s):  
F. E. Sieber ◽  
P. R. Brown ◽  
Y. Wu ◽  
R. C. Koehler ◽  
R. J. Traystman

The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMRO2) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; non-diabetic acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 +/- 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 micrograms/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 +/- 0.3, 14.9 +/- 2.5, 3.3 +/- 0.8, and 13.3 +/- 0.7 mM, respectively, at control. The corresponding baseline CMRO2 levels were 2.8 +/- 0.2, 3.0 +/- 0.2, 4.1 +/- 0.4, and 4.0 +/- 0.3 ml O2.100 g-1 x min,1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 +/- 3, 50 +/- 3, 51 +/- 3 vs. 36 +/- 1 ml x 100 g-1 x min-1) and cerebrovascular resistance was lower (2.24 +/- 0.15, 2.51 +/- 0.14, 2.38 +/- 0.21 vs. 3.35 +/- 0.18 mmHg.ml-1 x 100 g.min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
Kelsey R. Thomas ◽  
Alexandra J. Weigand ◽  
Isabel H. Cota ◽  
Emily C. Edmonds ◽  
Christina E. Wierenga ◽  
...  

AbstractRegional cerebral blood flow (CBF) has a complex relationship with cognitive functioning such that cognitively unimpaired individuals at risk for Alzheimer’s disease (AD) may show regional hyperperfusion, while those with cognitive impairment typically show hypoperfusion. Diabetes and word-list intrusion errors are both linked to greater risk of cognitive decline and dementia. Our study examined associations between fasting blood glucose, word-list intrusion errors, and regional CBF. 113 cognitively unimpaired older adults had arterial spin labeling MRI to measure CBF in a priori AD vulnerable regions: medial temporal lobe (MTL), inferior parietal lobe (IPL), precuneus, medial orbitofrontal cortex (mOFC), and pericalcarine (control region). Hierarchical linear regressions, adjusting for demographics, vascular risk, and reference CBF region, examined the main effect of blood glucose on regional CBF as well as whether intrusions moderated this relationship. Higher glucose was associated with higher CBF in the precuneus (β = .134, 95% CI = .007 to .261, p = .039), IPL (β = .173, 95% CI = .072 to .276, p = .001), and mOFC (β = .182, 95% CI = .047 to .320, p = .009). There was no main effect of intrusions on CBF across regions. However, the glucose x intrusions interaction was significant such that having higher glucose levels and more intrusion errors was associated with reduced CBF in the MTL (β = -.186, 95% CI = -.334 to -.040, p = .013) and precuneus (β = -.146, 95% CI = -.273 to -.022, p = .022). These findings may reflect early neurovascular dysregulation, whereby higher CBF is needed to maintain unimpaired cognition in individuals with higher glucose levels. However, lower regional CBF in unimpaired participants with both higher glucose and more intrusions suggests a failure in this early compensatory mechanism that may signal a decrease in neural activity in AD vulnerable regions.


2020 ◽  
Vol 6 (3) ◽  
pp. 149
Author(s):  
Indi Kamilia Fitri ◽  
Cholis Abrori ◽  
Dion Krismashogi Dharmawan

In people with diabetes mellitus (DM) there is a decrease in basal vitamin C levels which is thought to be a result of oxidative stress in the condition of hyperglycemia that it needs to increase vitamin C as an antioxidant. Hyperglycemia in DM needs to be lowered by pharmacological therapy, named glimepirid so the purpose of this study is to determine the effectiveness of vitamin C addition to the reduction of KGD hyperglycemic mice with glimepirid treatment. This study is true experimental with a sample of 25 mice 20-30 grams and divided into five groups, first the control group (K0); STZ  induction group (K1); STZ induction group with glimepirid treatment (K2); STZ induction group with the treatment of vitamin C (K3); STZ induction group by treatment of a combination of glimepirid and vitamin C (K4). STZ is injected intraperitonially 150 mg / kgBB. All groups were measured for KGD 1 after induction of STZ and KGD 2 after treatment for fourteen days. The results of the STZ induction group with the treatment of a combination of glimepirid and vitamin C (K4) experienced a smaller and not significant decrease in BSL in the STZ induction group with a single glimepirid (K2) treatment. These results are thought to have an influence from interactions between drugs that cause one drug to not work optimally. The conclusion of this study is that administration of glimepirid, vitamin C, or both can reduce blood glucose levels in hyperglycemic mice with the greatest decrease occurring in the glimepirid group.


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