3.5 Effect of PA extract on biochemical parameters
Plasma insulin is one of the essential factors for estimation sugar
associated with diabetes. Several researchers suggested that the plasma
insulin level reduces during the expansion of diabetes due to break down
of pancreatic β-cells. The plasma insulin level was almost same in
normal and PA (200 mg/kg) group rats. STZ induced DM rats showed
the reduction in plasma insulin that may be attributed to dysfunction of
pancreatic β-cells. DM rats treated with PA showed the
significantly (p<0.001) enhancement of plasma insulin level in
dose-dependent manner. STZ group rats demonstrated the plasma insulin
3.1±0.32 (μU/mL), which was less than 4 times as compared to normal andPA (200 mg/kg) group rats. PA treatment showed the insulin
level as 5.05±0.93, 8.13±0.56 and 12.54±0.85 (μU/mL), respectively
(Supplementary table 5). The results suggest that PA improved the plasma
insulin and decrease the BGL and confirms its anti-diabetic effect.
A similar style was observed in case of hexokinase content. The
hexokinase level was decreased in the STZ induced DM group rats and does
depend on the treatment of PA significantly (p<0.001)
(Supplementary table 5).
The level of glycated Haemoglobin, fructose-1-6-biphosphatase, and
glucose-6-Phosphatase was increased in the STZ induced DM group rats,
which was significantly (p<0.001) down-regulated by thePA in t a dose-dependent manner (Supplementary table 5).
Supplementary table 6 illustrates the effect of the PA on the
HOMA IR and HOMA β. HOMA IR level of DC control group rats increased and
the level of HOMA β reduced in the DC group rats, the dose-dependent
treatment of PA altered the level of HOMA IR and HOMA β a
resemblance with glibenclamide treated group.
The liver tissue plays a crucial role in the circulation of glucose in
various pathological and physiological states especially in case of
diabetes. Several drugs, compounds, and many more products are
detoxified and metabolized in the liver by a different mechanism (Ahmed
et al., 2013, 2014b; Kumar et al., 2014). Existing literature suggests
that diabetes directly linked to the variety of hepatic abnormalities
such as fibrosis, glycogen deposition, increased non-alcoholic fatty
liver disease (NAFLD), liver enzymes, Hepatocellular carcinomas,
cirrhosis, viral hepatitis, acute liver disease and fibrosis to name
few. One important role by the liver is well associated with control of
postprandial hyperglycemia and glycogen synthesis. The liver enzymes
such as fructose-1-6-biphosphatase, Hexokinase and glucose-6-phosphate
play a vital role during the conversion of glucose to required energy,
glycogen synthesis and glucose utilization (Tappy and Lê, 2012). Several
research suggests that the reduced level of hexokinase increase the
glucose level into the circulating blood via inhibiting the conversion
of glucose into glucose-6-phosphate (Newsholme et al., 1968). Our
results of STZ induced DM group rats and PA -treated group rats
showed the increased level of hexokinase, responsible for its
anti-diabetic effects. glucose-6-phosphate is regulated during glucose
metabolism with the help of hexokinase. Increase level of
glucose-6-phosphate, can be related to its increase gluconeogenetic
enzyme activity and boost the production of fats and in renal and
hepatic tissue (Ahmed et al., 2013, 2014c, 2015; Kumar et al., 2013,
2014). Fructose-1,6 biphosphatase and glucose-6-phosphatase, both play a
key role in the gluconeogenic pathway, in diabetes, there is increased
synthesis of both these enzymes, responsible for increasing the glucose
production by the tissue. STZ induced DM rats showed the increased
activity of both enzymes and dose-dependent treatment of PAshowed the reduction of the activity in fructose-1,6 biphosphatase and
glucose-6-phosphatase. These results confirm and suggest the
anti-diabetic effect of PA . The possible mechanism may be due to
the reduction of the glyconeogenesis and increase glycolysis.