BACKGROUND: Okra (Abelmoschus esculentus (L.) Moench) is traditionally used by different populations of Africa, América, Asia, and Europa to control diabetes. Although its action has been evaluated in several preclinical rodent trials, they have not been systematically analyzed.
OBJECTIVE: To evaluate the effectiveness of using okra in the treatment of diabetes in experimental rodent models.
METHODS: Controlled and randomized rodent animal trials with induced diabetes published between January 2000 and January 2021 were searched in the PubMed, Scopus, Scielo, and Web of Science databases. The search strategy included studies comprising the descriptors: animal species, diabetes induction method, intervention time, part of okra fruit used (whole, seeds, or peels), and dose as well as observed effects on biochemical and metabolic parameters. The systematic review was carried out according to the PRISMA statement, Cochrane bias risk tool (SYRCLE\'s RoB tool), and registered for systematic review protocols (PROSPERO).
RESULTS: A total of 326 articles were identified and after the exclusion of studies with gestational animal models, non-rodent animals, and non-diabetic animals, 11 studies involving 388 rodents were selected for the synthesis of results. The diabetes induction methods included streptozotocin, streptozotocin-nicotinamide, alloxan monohydrate, insulin resistance by high-fat diets or formulation described in AIN - 76, and feeding with high-fat food. Both Wistar albino rats, Sprague-Dawley males, and rats of both sexes of the Long-Evans lineage as well as male albino mice and C57BL females were included in the experiments. Studies showed that extracts of the fruit, the fresh fruit, or its various fractions had positive effects on the following markers: glycated hemoglobin, cholesterol, HOMA-IR, oral glucose tolerance test, and blood glucose, in acute (2 and 24 h), and chronic (up to 4 months) treatment.
CONCLUSIONS: An important hypoglycemic effect of okra in its various fractions on induced diabetes was observed by different authors. Moreover, okra promoted improvement in metabolic markers such as insulin sensitivity, lipid profile, and bodyweight loss.

The present paper provides a comprehensive review of latent extinction. In maze learning situations, latent extinction involves confining an animal to a previously reinforced goal location without food. When returned to the starting position after latent extinction, the animal typically shows a response decrement. Such findings have suggested that latent extinction is sufficient to invoke extinction learning, despite the animal having been prevented from making the original response. The majority of research on latent extinction was conducted between 19491980 and focused on what is being learned during the latent placements. Stimulus-response (S-R) theorists attempted to explain latent extinction via novel S-R mechanisms, namely, the fractional anticipatory response (rG). However, research did not support the role of rG in latent extinction. Cognitive expectancy theorists provided a simpler, more adequate explanation for latent extinction, more consistent with the data. Specifically, latent extinction might instill a change in expectation (i.e., animals learn to expect absence of reinforcement). Evidence also suggests that latent extinction involves place learning mechanisms and is sensitive to modulation via certain experimental factors. More recent work has uncovered some of the neural mechanisms of latent extinction. The hippocampus is critically involved in latent extinction, whereas other brain regions typically implicated in regular \"response extinction\" in the maze, such as the dorsolateral striatum, are not required for latent extinction. Similar to other kinds of learning, latent extinction requires NMDA receptor activity, suggesting the involvement of synaptic plasticity. Consistent with a multiple memory systems perspective, research on latent extinction supports the hypothesis that extinction learning is not a unitary process but rather there are different kinds of extinction learning mediated by distinct neural systems.

Environmental enrichment (EE) for rodents is generally defined as providing subjects with an environment enhanced with access to conspecifics, novel and tactile stimuli, and in many preparations, more space. EE exposure, in particular as an \"intervention\" in adult rodents, decreases food and drug seeking and taking. This review focuses on the reduction of sucrose seeking and taking in rats assessed in operant-based procedures. The operant-based model provides a means to evaluate addiction-related behaviors. Findings using the model might translate to clinically-relevant addiction behaviors directed towards both drugs and food. Both overnight (acute) and one month (chronic) EE effects on behavior are described, including a recent evaluation of the persistence of EE effects following its removal. EE effects on neurobiology related to sucrose seeking using the model are outlined, with a special emphasis on meso-cortico-limbic terminals. Overall, our working hypothesis for how EE reduces sucrose seeking and taking is that EE alters processing of incentive valence. This may also be accompanied by changes in learning and affect. Anti-seeking and anti-taking effects of EE have translational implications for the prevention and treatment of both drug addiction and food-focused behaviors (\"food addiction\").