Type 2 Diabetes Mellitus in Low- and Middle-Income Countries: The Significant Impact of Short-Chain Fatty Acids and Their Quantification.

Globally, type 2 diabetes mellitus (T2DM) is a major threat to the public's health, particularly in low- and middle-income countries (LMICs). The production of short-chain fatty acids (SCFAs) by the gut microbiota has been reported to have the potential to reduce the prevalence of T2DM, particularly in LMICs where the disease is becoming more common. Dietary fibers are the primary source of SCFAs; they can be categorized as soluble (such as pectin and inulin) or insoluble (such as resistant starches). Increased consumption of processed carbohydrates, in conjunction with insufficient consumption of dietary fiber, has been identified as a significant risk factor for type 2 diabetes (T2DM). However, there are still controversies over the therapeutic advantages of SCFAs on human glucose homeostasis, due to a lack of studies in this area. Hence, a few questions need to be addressed to gain a better understanding of the beneficial link between SCFAs and glucose metabolism. These include the following: What are the biochemistry and biosynthesis of SCFAs? What role do SCFAs play in the pathology of T2DM? What is the most cost-effective strategy that can be employed by LMICs with limited laboratory resources to enhance their understanding of the beneficial function of SCFAs in patients with T2DM? To address the aforementioned questions, this paper aims to review the existing literature on the protective roles that SCFAs have in patients with T2DM. This paper further discusses possible cost-effective and accurate strategies to quantify SCFAs, which may be recommended for implementation by LMICs as preventive measures to lower the risk of T2DM.

Association of Carboxyhemoglobin Levels with Peripheral Arterial Disease in Chronic Smokers Managed at Dr George Mukhari Academic Hospital.

Chronic cigarette smokers (CCS) are known to have elevated levels of carboxyhemoglobin (COHb). However, it is not known whether increased levels of COHb are associated with endothelial dysfunction (ED), and therefore the development of peripheral arterial disease (PAD). The aim of the study was to investigate the association of blood COHb and plasma nitric oxide (NO) levels, and whether it is an independent risk factor in the development of PAD among CCS at Dr George Mukhari Academic Hospital (DGMAH). A sample of 120 CCS with PAD and a convenience sample of 100 CCS without PAD were recruited into the study. Blood COHb levels were measured using the ABL 90 FLEX CO-oximeter automated spectroscopy. Plasma nitric oxide (NO) levels were measure using ELISA. Logistic regression analysis was used to investigate the association of blood COHb and plasma NO with PAD. Blood COHb levels of CCS with PAD were significantly higher than those of CCS without PAD, and the NO levels of CCS with PAD were significantly lower than those of CCS without PAD. Although both the blood COHb and plasma NO in CCS were significantly associated with PAD in bivariate logistic analysis, only plasma NO was independently associated with PAD in multivariate logistic analysis. This finding is consistent with the hypothesis that COHb is a cause of arterial damage in PAD, leading to reduced NO, and therefore reduced arterial dilation.

The use of liver slices from the Cape vulture (Gyps coprotheres) to better understand the role of liver toxicity of non-steroidal anti-inflammatory drugs (NSAIDs) in vultures.

Diclofenac, a non-steroidal anti-inflammatory drug (NSAID) was responsible for the death of millions of vultures on the Asian subcontinent, following the consumption of diclofenac contaminated carcasses. The aim of this research was to establish if liver slices could serve as an alternate means of predicting the toxicity of NSAIDs in Gyps vultures. The Cape vulture liver slices was prepared and incubated with four NSAIDs for 6 h. A percent clearance of 1.0 ±â€¯0.253, 0.58 ±â€¯0.153, 0.961 ±â€¯0.312 and 1.242 ±â€¯0.406 (%/h*g) was attained for diclofenac, carprofen, ketoprofen and meloxicam respectively. Both meloxicam and diclofenac exerted toxic effects on the hepatic cells. Protein content indicated that the vulture tissue had lower enzyme levels than expected for an animal of its size. The poor distinction between the ex vivo hepatic percent clearance of meloxicam and diclofenac indicates that liver slices is not an ideal model to investigate NSAIDs toxicity in Cape vulture.

Technique for the collection of clear urine from the Nile crocodile (Crocodylus niloticus).

Urine samples can be a very useful diagnostic tool for the evaluation of animal health. In this article, a simple technique to collect urine from the Nile crocodile (Crocodylus niloticus) was described, based on a similar unpublished technique developed for the American alligator (Alligator mississippiensis) using a canine urinary catheter. With this technique, it was possible to collect relatively clean urine samples from Nile crocodiles of different sizes using canine urinary catheters or small diameter stomach tubes. Based on the gross anatomical features of the cloaca of the Nile crocodile, it was confirmed that urine accumulates in a chamber consisting of the urodeum and coprodeum. Faecal material is stored temporarily in the very short rectum, which is separated from the urinary chamber by the rectocoprodeal sphincter.

Removing the threat of diclofenac to critically endangered Asian vultures.

Veterinary use of the nonsteroidal anti-inflammatory (NSAID) drug diclofenac in South Asia has resulted in the collapse of populations of three vulture species of the genus Gyps to the most severe category of global extinction risk. Vultures are exposed to diclofenac when scavenging on livestock treated with the drug shortly before death. Diclofenac causes kidney damage, increased serum uric acid concentrations, visceral gout, and death. Concern about this issue led the Indian Government to announce its intention to ban the veterinary use of diclofenac by September 2005. Implementation of a ban is still in progress late in 2005, and to facilitate this we sought potential alternative NSAIDs by obtaining information from captive bird collections worldwide. We found that the NSAID meloxicam had been administered to 35 captive Gyps vultures with no apparent ill effects. We then undertook a phased programme of safety testing of meloxicam on the African white-backed vulture Gyps africanus, which we had previously established to be as susceptible to diclofenac poisoning as the endangered Asian Gyps vultures. We estimated the likely maximum level of exposure (MLE) of wild vultures and dosed birds by gavage (oral administration) with increasing quantities of the drug until the likely MLE was exceeded in a sample of 40 G. africanus. Subsequently, six G. africanus were fed tissues from cattle which had been treated with a higher than standard veterinary course of meloxicam prior to death. In the final phase, ten Asian vultures of two of the endangered species (Gyps bengalensis, Gyps indicus) were dosed with meloxicam by gavage; five of them at more than the likely MLE dosage. All meloxicam-treated birds survived all treatments, and none suffered any obvious clinical effects. Serum uric acid concentrations remained within the normal limits throughout, and were significantly lower than those from birds treated with diclofenac in other studies. We conclude that meloxicam is of low toxicity to Gyps vultures and that its use in place of diclofenac would reduce vulture mortality substantially in the Indian subcontinent. Meloxicam is already available for veterinary use in India.