Sheanut (Butyrospernum paradoxum) is an oil rich tropical tree crop, which is indigenous to
the West African savannah zone. In Nigeria, most of the sheanuts shelling are done manually
by rural women and children, which is labour demanding and tedious. This research work
was carried out to determine some physical and mechanical properties of sheanut in order
to minimize economic losses associated with its processing. The mean values recorded
for the physical properties at 25% moisture content (wb) are; major diameter (29.20 mm),
intermediate diameter (21.90 mm), minor diameter (15.00 mm), geometric mean diameter
(21.90 mm), arithmetic mean diameter (21.20 mm), angle of repose (30.280). The mean
values for the mechanical properties are; linear limit force (0.80 kN), linear limit deformation
(4.60 mm), bioyield point force (1.40 kN), bioyield point deformation (6.50 mm), rupture
point force (2.10 kN) and rupture point deformation (9.60 mm). Based on the physical and
mechanical properties, a sheanut shelling machine was developed that is capable of addressing
the aforementioned problems. Putting into consideration better shelling and efficient separation
of shea nuts so as to encourage more utilization and processing of shea nuts and its products.
The machine was designed to be powered by 5 hp electric motor. It was tested to shell, separate
and clean sheanuts. The result of the performance evaluation showed that the machine had
shelling efficiency of 96%; cleaning efficiency of the machine was 69.56% while the recovery
efficiency was 82.7%. The successful development of this machine will reduce drudgery and
time taken associated with the traditional method of sheanut shelling and therefore will increase
productivity and utilization.
The role of the endoplasmic reticulum (ER) has evolved from protein synthesis, processing, and other secretory pathways to forming a foundation for lipid biosynthesis and other metabolic functions. Maintaining ER homeostasis is essential for normal cellular function and survival. An imbalance in the ER implied stressful conditions such as metabolic distress, which activates a protective process called unfolded protein response (UPR). This response is activated through some canonical branches of ER stress, i.e., the protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6 (ATF6). Therefore, chronic hyperglycemia, hyperinsulinemia, increased proinflammatory cytokines, and free fatty acids (FFAs) found in diabesity (a pathophysiological link between obesity and diabetes) could lead to ER stress. However, limited data exist regarding ER stress and its association with diabesity, particularly the implicated proteins and molecular mechanisms. Thus, this review highlights the role of ER stress in relation to some proteins involved in diabesity pathogenesis and provides insight into possible pathways that could serve as novel targets for therapeutic intervention.
The endoplasmic reticulum (ER) plays a multifunctional role in lipid biosynthesis, calcium storage, protein folding, and processing. Thus, maintaining ER homeostasis is essential for cellular functions. Several pathophysiological conditions and pharmacological agents are known to disrupt ER homeostasis, thereby, causing ER stress. The cells react to ER stress by initiating an adaptive signaling process called the unfolded protein response (UPR). However, the ER initiates death signaling pathways when ER stress persists. ER stress is linked to several diseases, such as cancer, obesity, and diabetes. Thus, its regulation can provide possible therapeutic targets for these. Current evidence suggests that chronic hyperglycemia and hyperlipidemia linked to type II diabetes disrupt ER homeostasis, thereby, resulting in irreversible UPR activation and cell death. Despite progress in understanding the pathophysiology of the UPR and ER stress, to date, the mechanisms of ER stress in relation to type II diabetes remain unclear. This review provides up-to-date information regarding the UPR, ER stress mechanisms, insulin dysfunction, oxidative stress, and the therapeutic potential of targeting specific ER stress pathways.