Occurrence of mild cognitive impairment with hyperinsulinaemia in Africans with advanced type 2 diabetes mellitus.

There is paucity of information on the prevalence of mild cognitive impairment (MCI) among individuals with type 2 diabetes mellitus (T2DM) in sub-Saharan Africa, including Nigeria. In addition, the role of hyperinsulinaemia in the development of MCI needs further investigation. This study sought to assess cognition and hyperinsulinaemia, with the associated characteristics in patients with advanced T2DM. Cognition was assessed using Montreal cognitive assessment test (MoCA), while fasting plasma insulin was measured using an ELISA kit. Sixty one diabetic subjects and 32 non-diabetic controls, matched for age, gender and level of education were studied. The diabetics had MCI while the controls had normal cognitive function. About 88.5% of the diabetic subjects had MCI, in contrast with only 50% of the non-diabetic controls. The most significantly affected cognitive domains among the diabetics were executive function, naming, attention, abstraction and delayed recall. Among the diabetics, MCI correlated with age, weight and body mass index (BMI); and in addition, age and weight found to be significant predictors of MCI. Plasma insulin concentration among the diabetics (16.24 ± 13.5 µIU/ml) was more than twice that of the controls (7.59 ± 2.9 µIU/ml). Hyperinsulinaemia among the diabetics correlated with weight, BMI, blood pressure and fasting blood sugar (FBS). Glycated haemoglobin and FBS levels were higher among diabetics compared with the controls. In conclusion, Africans with advanced T2DM show multi-domain MCI with high prevalence, coexisting with hyperinsulinaemia. Majority of the patients have diabetic complications and poor glycaemic control. Hyperinsulinaemia may play a complementary role in the pathophysiology of MCI in T2DM.

Raised high-sensitivity C-reactive protein and cognitive impairment among African stroke survivors within the first three months following stroke.

Stroke remains a major factor causing death and disabilities such as cognitive impairment. There is conflicting evidence on the role and dynamics of high sensitivity C-reactive protein (hsCRP), an acute phase pro-inflammatory protein, in post-stroke cognitive impairment. This study evaluated cognitive impairment and examined its relationship with serum hsCRP in the first three months following stroke. Cognition was assessed using Montreal Cognitive Assessment test, while serum hsCRP concentrations were assessed using enzyme link immunosorbent assay kit. Data were processed using SPSS Statistics version 20.0. Sixty subjects, comprising of 30 stroke patients and 30 healthy subjects, matched for age, sex and level of education were studied. Cognitive impairment was observed among the stroke patients, while the healthy subjects showed normal cognitive function; and the difference in the cognitive scores of the two groups was highly significant (P = 0.001). There was higher prevalence of cognitive impairment among the stroke survivors compared to the non-stroke subjects. Serum hsCRP was significantly higher among the stroke survivors compared to the healthy subjects (P = 0.001). The high hsCRP level correlates well with duration of stroke and working memory domain of cognition. The data revealed a high prevalence of cognitive impairment and concurrent high serum hsCRP levels among stroke survivors in the first three months following stroke, in contrast with normal subjects. The high hsCRP level correlates with duration of stroke and working memory domain of cognition. The data suggest a role for serum hsCRP and inflammation in the development of post-stroke cognitive impairment.

Effect of Caffeine on Serum Tumour Necrosis Factor Alpha and Lactate Dehydrogenase in Wistar Rats Exposed to Cerebral Ischaemia-reperfusion Injury.

Caffeine is known to confer neuro-protection via A1 and A2A adenosine receptor antagonism in which adenosine neuro-modulates excitotoxic release of glutamate. Currently, it is unclear whether caffeine modulates inflammation in ischaemic stroke model. The present study examined effects of caffeine following ischaemia-reperfusion injury on neuro-inflammatory tumour necrosis alpha (TNF-α), lactate dehydrogenase (LDH), as well as effect of caffeine against brain ischaemic damage on histology. Thirty three adult male Wistar rats (180-300 g) were used in this study. They were randomly divided into four groups (n=5 each): Group I (Control) that received neither the operation nor any treatment; Group II (Sham/Water) received a pseudo-ischaemic-reperfusion and 1ml water for injection; Group III (BCCO/Water) that received complete bilateral common carotid occlusion (BCCO) and 1ml water for injection; Group IV (BCCO/Caffeine) that received complete BCCO and caffeine solution intraperitoneally at a dose of 50% LD50 value (144mg/kg); and thirteen rats were used for LD50 assessment. Sensory and motor functions significantly (p<0.05) decreased in the rat following ischaemia-reperfusion injury when compared to pre-injury state on Garcia neurological score. Caffeine reduced brain ischaemic injury and significantly reduced (p<0.05) TNF-α activity. While no significant effects (p>0.05) of caffeine was observed on LDH activity. This study has shown neuro-protective roles of caffeine against ischaemia-reperfusion damage to brain tissue, inflammatory TNF-α activity, but not on LDH activity.

Disturbances in Calcium and Zinc Homeostasis During Testicular Damage Induced by Citrus aurantifolia Juice in Wistar Rats.

Infertility rate is high globally and in Nigeria. The reported spermicidal activity of Citrus aurantifolia juice (CAJ)and its popular consumption may be a contributing factor to the rise in male infertility. This study examined the effects ofCAJ on testis and evaluated the role of calcium and zinc in these effects. Twenty-eight male rats (200-220g) were groupedinto four (n=7). Group I (control) received 0.5ml normal saline, while groups II, III and IV received 600mg/kg, 900mg/kgand 1200mg/kg of CAJ, respectively, orally for 35 days. Sperm analysis, testicular histology, testicular zinc and calciumconcentrations were evaluated. The results showed a significant decrease (P < 0.001) in body weight and gonad-somaticindex (GSI) of the rats in group IV. No sperm cells were found in the sperm samples of all the treatment groups in contrastto control. There was a significant decrease (P < 0.001) in zinc concentration of group III and IV animals and a significantincrease (P < 0.001) in testicular calcium content of group III and IV animals. Derangement of testicular cyto-architecture,shrinkage or complete destruction of seminiferous tubules as well as absence of spermatogenic cells were observed in thetreatment groups. It was concluded that CAJ induced a destructive effect on testes of rats as evidenced by damaged testiculartissue, reduced gonado-somatic index, azospermia and disruption in testicular electrolyte homeostasis. It was concluded thatCAJ caused hypercalcaemia and hypozincaemia in the testicular tissue of the treated rats. Concurrently, CAJ also causeddamage to testicular histology, azospermia and decreased GSI. Citrus aurantifolia juice should be consumed with cautiondue to its potential to cause infertility in males.

Effect of Insulin on Visuo-Spatial Memory and Histology of Cerebral Cortex in the Presence or Absence of Nitric Oxide Inhibition.

Insulin has emerged from its traditional 'peripheral' glucose-lowering function to become increasingly regarded as a brain hormone that controls a wide range of functions including learning and memory. Insulin action on learning and memory is linked to nitric oxide (NO) signalling, but its effects on memory and histology of cerebral cortex in conditions of varied NO availability is unclear. This research sought to determine the effect of insulin on visuo-spatial learning, memory and histology of cerebral cortex during NO deficiency. Twenty-four mice weighing 21-23 g, were divided into four groups (n = 6) and treated daily for seven days with 0.2 ml distilled water subcutaneously (s.c.) (control), 10 I.U/kg insulin s.c., 10 I.U/kg insulin + 50 mg/kg L-NAME intraperitoneally (i.p.), and 50 mg/kg i.p. L-NAME s.c., respectively. The 3-day MWM paradigm was used to assess memory. Brain tissue was examined for histological changes. There was no significant difference between day 1 and day 2 latencies for all the groups. The mice in all (but L-NAME) groups spent more time in the target quadrant, and the difference was significant within but not between groups. There was significant reduction in number of platform site crossings (4.83 ± 0.5, 0.67 ± 0.3, 0.50 ± 0.3 and 0.50 ± 0.3 for control, insulin, insulin+L-NAME and L-NAME groups, respectively) in all the groups compared to control. Normal histology of the cortex and absence of histological lesions were observed in brain slides of control and treatment groups. It was concluded that insulin administration impairs visuo-spatial memory to a greater extent in the presence of NO block, and to a lesser extent in the absence of NO block. Nitric oxide has a role in insulin-induced memory impairment. Insulin administration in the presence or absence of NO block had no effect on histology of cortex.