**1. Introduction**

Obesity is now a global burden [1, 2]. Increase in the prevalence of obesity has lead the American Heart Association (AHA) to call for actions to prevent the consequences of this epidemic [3, 4]. Recently, the AHA reviewed many weight-loss approaches for the management and treatment of obesity [5].

Foods such as fats, carbohydrates or sugar are considered to be causes of such increase in global obesity pandemic. Intakes of carbohydrates result in increase in release of insulin which suppresses the release of fatty acids into circulation, thus storage of fat in fat cells. So carbohydrate is blamed for increase in obesity.

The German Nutrition Society published guidelines in which relationships between carbohydrate intake and prevention of nutrition-related diseases are indicated [6]. The guideline proposes that high carbohydrate intake at the expense of total fat and saturated fatty acids reduces the concentrations of total, LDL, and HDL

cholesterol. A high carbohydrate consumption at the expense of polyunsaturated fatty acids such as EPA or DHA increases total and LDL cholesterol. But reduces HDL cholesterol. Further, intake of high carbohydrate increases triglyceride concentration. High consumption of sucrose increases obesity and type2 diabetes mellitus (T2DM).

On the other hand, as stated later, glucose is needed for many brain functions such as memory, emotion, decision, motivation etc. Sucrose is degraded in the intestine and gives rise to glucose. Some studies show that sucrose intakes improve memory.

In the present review, we discuss the transportation of glucose from the blood to the brain, influences of glucose or sucrose on memory and working ability, and feeding.

### **2. Importance of glucose in the brain functions**

It is now well known that glucose is important for a variety of brain functions. Late 20th century, the development of positron emission tomography (PET) made it possible to visualize the amount of glucose in discrete regions of the brain. For example, light stimulation increased the metabolism of cerebral glucose in the primary visual cortex [7].

The learning of a complex visuospatial motor task was shown to increase the use of glucose by the brain [8].

Summarizing data published, PET studies showed that cognitive demand increased glucose metabolism in localized regions of the brain. In PET studies radioactively labeled glucose appears in brain areas that are metabolically active within a few minutes after the injection into blood. These observations indicate that the brain relies on glucose when neurons are activated.

#### **2.1 Transportation of glucose from blood to brain**

Tsacopoulos et al. [9] indicated that capillaries of the brain are surrounded by glia cells and glucose uptaken is phosphorylated exclusively in glia cells, not in neurons.

In mammalian there is evidence that glutamate is a coupling signal between neuronal activation and glucose uptake by astrocytes [10, 11].

Astrocytes surround capillaries, which indicate that astrocytes form the first cellular barrier that glucose encounters in the brain. This suggests that astrocytes are likely sites of primary glucose uptake (**Figure 1**).

Schematic figure of the cytological relationships among capillary, astrocyte, and neuron. Processes of astrocytes surround capillaries (end-feet) and ensheath synapses. Receptors and uptake sites for neurotransmitters are on astrocytes. Astrocytes are ideally suited to sense synapse activity and to couple it with glucose uptake and its metabolism.

There are glucose transporters (55kDA Glut1) in the inner sites and outer sites of endothelial cells, and between astrocytes and capillaries (45kDA Glut1). There are Glut 3 transporters on walls of neurons [12].

Glut 1 and Glut 3 glucose transporters are present in the walls of capillaries and neurons (**Figure 2**).

Glucose transporters, Glut1 are located in the luminal and abluminal membranes of brain endothelial cells. There are small amounts of Glut 1 located in the cytoplasm and the largest fractions of Glut1 are at the abluminal membranes. The lower content of Glut1 at the luminal membrane may be due to the comparably high glucose concentration in this membrane, which is close to the plasma concentration.

There appears to be a tight coupling between Na<sup>+</sup> dependent glutamate uptake by astrocytes and glucose utilization [13] (**Figure 3**).

*Roles of Glucose and Sucrose Intakes on the Brain Functions Measured by the Working Ability… DOI: http://dx.doi.org/10.5772/intechopen.99203*

**Figure 1.** *Capillary, astrocyte and neuron.*

**Figure 2.** *Glucose transporters in the walls of capillaries and the walls of neuron.*

Glutamate is cotransported with Na<sup>+</sup> , causing increase in the concentration Na<sup>+</sup> in astrocytes, which activate the astrocyte Na+ /K+ -ATP ace. Activation of Na+ /K+ - ATPase stimulates glycolysis. Lactate released by astrocytes is taken up by neurons and become energy source of neurons.

When summarized, glucose is degraded by glycolysis in astrocytes which generates two molecules of ATP used for uptake of K+ and glutamate from the synaptic cleft. When neurons are active, glycolysis is more active, so that transportation of glucose from the blood to astrocytes increases.

### **2.2 Roles of glucose in memory**

It has been known long time that glucose intake improves cognitive behaviors. In elderly humans, changes in blood glucose levels following ingestion of a glucose containing drink was shown to be significantly correlated with performances in the Wechsler memory scale [14].

#### **Figure 3.**

*Transportation of glucose from the blood to neurons.*

Verbal fluency of a group of 80 females, aged 20, was measured after taking a glucose drink or placebo. The fluency was significantly higher after a glucose drink [15].

It was shown that an equilibrium starts between the level of glucose between blood and brain [16]. Such mechanism suggests that higher blood glucose levels promote better performance of brain functions.

The recall of a story was associated with blood glucose levels measured by Wechsler memory scale [17]. A positive correlation between blood glucose and forgetting was shown in young adults, thus those with higher initial blood glucose remember more.

There are various data indicating that glucose supply to the brain is necessary for maintaining good performances of brain functions.

In rats, systemic injections of glucose were shown to enhance learning and memory in many conditions. When microinjected into the specific sites of the brain, glucose levels increased and improved behavioral performances controlled by these sites [18].

Furthermore, glucose administration was shown to enhance memory in generally healthy aged rodents and humans. Glucose ingestion resulted in significant enhancement of performances on several tests including orientation, word recognition, and recall, narrative prose, and face recognition [19].

#### **2.3 Glucose and memory measured by Morris maze experiments**

As stated above, glucose intakes improve brain functions. Sucrose is degraded to glucose in the intestine and glucose is transported to the blood. A few systematic studies have been carried out as to the effects of sucrose on brain function [20, 21].

Morris used the delayed matching-to-place task which is an unusual variant of the water-maze protocols [22].

#### *2.3.1 Experimental procedures*

Wistar rats aged 11 weeks were trained in water to learn the location of the platform. Rats later learned to reach the platform in 15 min. After 6–12 trials. Rats were *Roles of Glucose and Sucrose Intakes on the Brain Functions Measured by the Working Ability… DOI: http://dx.doi.org/10.5772/intechopen.99203*

administered either glucose (2 g/8 ml/kg) or 8 ml/kg of water intraperitoneally. 24 hours later rats swam in Morris water maze and the ratio of stay at the platform (target) quarter to the rest of the area was measured. The distance to the target was also compared between glucose administered rats and the controls.

### *2.3.2 Results*

**Figure 4** show that the ratio of stay in the target quarter in the test was larger after glucose was given, but data are not statistically significant.

Rats were given sucrose solution (10%) or sucralose solution (0.015%) or water as a control in a drinking bottle.

**Figure 4.**

*Effects of glucose administration on memory [23].*

**Figure 5.**

*Effects of sucrose administration on the improvement of memory.*

**Figure 5** shows that rats given sucrose stayed at the target quarter significantly more compared with rats given sucralose. There was no significant decrease about the proximity measurements between rats given sucrose and sucralose.

These results clearly show that the administration of sucrose improved memory consolidation when compared with rats given sucralose in Morris maze experiments.
