ABSTRACT
BACKGROUND: Undernutrition is the most dominant form of malnutrition among children in developing countries. Studies conducted in Tanzania have reported high levels of undernutrition among children below five years of age. However, there is limited information on differences in stunting prevalence across agroecological zones. This study aimed to determine the prevalence of undernutrition and its determinants in the lowland and highland areas in Kilosa District, Tanzania. METHODS: A cross-sectional study was conducted in a sample of 200 randomly selected households from the lowland and 141 from the highland areas of Kilosa District in Morogoro Region, Tanzania. Sociodemographic, feeding practices, hygiene, and sanitation data were collected using a structured questionnaire. Weight and height of children were measured using a standard procedure, and age was calculated from the birth date obtained from the child growth card. Anthropometric data were analyzed by using Emergency Nutrition Assessment (ENA) software. The logistic regression model was used to explore the determinants of undernutrition. RESULTS: Prevalence of stunting, underweight, and wasting was 41.0%, 11.5%, and 2.5% in lowland and 64.5%, 22.0%, and 1.4% in highland areas, respectively. The prevalence of stunting and underweight was higher in the highland compared to the lowland areas (p < 0.001). Significant determinants of underweight were areas of residence (AOR 4.21, 95% CI: 1.62-10.9), age of the children (AOR 5.85, 95% CI: 1.81-18.97), and child birth weight (AOR, 4.98 95% CI: 1.65-15.05), while determinants of stunting were the area of residence (AOR, 2.77 95% CI: 1.43-5.36), maternal age (AOR, 0.33 95% CI: 0.14-0.79), sex of a child (AOR, 1.89 95% CI: 1.03-3.50), and child birth weight (AOR, 3.29 95% CI: 1.21-8.97). CONCLUSION: The prevalence of undernutrition, especially stunting and underweight, was high in the study areas. Determinants of stunting differed between highlands and lowland areas, highlighting the needs of having properly integrated interventions based on the geographical location.
ABSTRACT
Rat P23 is an isoform of trypsin (ogens) synthesized by rat acinar cells. Expression of P23 is stimulated strongly by caerulein, an analogue of cholecystokinin (CCK). However, the physiological relevance of rat P23 in healthy and pathological conditions such as caerulein-induced pancreatitis is largely unknown. Using recombinant P23 trypsinogen and reconstitution analysis of zymogen autoactivation, unique inhibitor-resistance characteristics of P23 were elucidated. P23 cDNA was expressed in Escherichia coli periplasm, yielding recombinant P23 trypsinogen. Autoactivation of zymogen granule contents from caerulein-induced rat pancreas was also studied. Activation kinetics of P23 by enterokinase was similar to those of rat anionic trypsinogen, which is a major isoform of trypsinogen. Interestingly, rat pancreatic secretory trypsin inhibitor (PSTI), which protects against deleterious activation of trypsinogens in zymogen granules, failed to inhibit P23 trypsin even with four-fold molar excess, at which concentration it effectively inhibited rat anionic trypsin to almost 100%. P23 trypsin also showed marked resistance to proteinaceous trypsin inhibitors such as soybean trypsin inhibitor and aprotinin. P23 trypsin activated by enterokinase dramatically accelerated the cascade of autoactivation of anionic trypsinogen even in the presence of PSTI. Taken together with a previous observation that P23 is specifically upregulated 14-fold by 24-h caerulein infusion, these results suggest that elevated levels of P23 should be taken into consideration in the mechanism of trypsinogens within the pancreas in pathological conditions.
