Neonatal intake of oleanolic acid attenuates the subsequent development of high fructose diet-induced non-alcoholic fatty liver disease in rats.

Dietary manipulations during the early postnatal period are associated with the development of metabolic disorders including non-alcoholic fatty liver disease (NAFLD) or long-term protection against metabolic dysfunction. We investigated the potential hepatoprotective effects of neonatal administration of oleanolic acid (OA), a phytochemical, on the subsequent development in adulthood, of dietary fructose-induced NAFLD. Male and female suckling rats (n=112) were gavaged with; distilled water (DW), OA (60 mg/kg), high fructose solution (HF; 20% w/v) and OA+HF (OAHF) for 7 days. The rats were weaned onto normal rat chow on day 21 up to day 55. From day 56, half of the rats in each treatment group were continued on plain water or HF as drinking fluid for 8 weeks. Hepatic lipid accumulation and hepatic histomorphometry were then determined. Fructose consumption in adulthood following neonatal fructose intake (HF+F) caused a 47-49% increase in hepatic lipid content of both male and female rats (P<0.05). However, fructose administered in adulthood only, caused a significant increase (P<0.05) in liver lipid content in females only. NAFLD activity scores for inflammation and steatosis were higher in the fructose-fed rats compared with other groups (P<0.05). Steatosis, low-grade inflammation and fibrosis were observed in rats that received HF+F. NAFLD area fraction for fibrosis was three times higher in rats that received fructose neonatally and in adulthood compared with the rats in the negative control group (P<0.05). Treatment with OA during a critical window of developmental plasticity in rats prevented the development of fructose-induced NAFLD.

Effect of neonatal orally administered S-allyl cysteine in high-fructose diet fed Wistar rats.

S-allyl cysteine (SAC) has antioxidant, antidiabetic and antiobesity properties. We hypothesized that neonatal oral administration of SAC would protect rats against neonatal and adulthood high-fructose diet-induced adverse metabolic outcomes in adulthood. In total, 112 (males=56; females=56), 4-day-old Wistar rat pups were randomly allocated to groups and administered the following treatment regimens daily for 15 days from postnatal day (PND) 6-20: group I - 10 ml/kg distilled water, group II - 10 ml/kg 20% fructose solution (FS), group III - 150 mg/kg SAC and group IV - SAC+FS. On PND 21, the pups were weaned and allowed to grow on a standard rat chow (SRC) until PND 56. The rats from each treatment regimen were then randomly split into two subgroups: one on a SRC and plain drinking water and another on SRC and 20% FS as drinking fluid and then subjected to these treatment regimens for 8 weeks after which they were euthanized and tissues collected for analyzes. Neonatal oral administration of SAC attenuated the neonatal high-fructose diet-induced programming for hepatic lipid accretion in adulthood but not against adulthood high-fructose diet-induced visceral obesity. Neonatal oral administration of SAC programmes for protection against neonatal fructose-induced programming for hepatic lipid accumulation thus could potentially protect against fat-mediated liver derangements in adult life.

Superficial brachial artery: a possible cause for idiopathic median nerve entrapment neuropathy.

Nerve entrapment syndromes occur because of anatomic constraints at specific locations in both upper and lower limbs. Anatomical locations prone to nerve entrapment syndromes include sites where a nerve courses through fibro-osseous or fibromuscular tunnels or penetrates a muscle. The median nerve (MN) can be entrapped by the ligament of Struthers; thickened biceps aponeurosis; between the superficial and deep heads of the pronator teres muscle and by a thickened proximal edge of flexor digitorum superficialis muscle. A few cases of MN neuropathies encountered are reported to be idiopathic. The superficial branchial artery (SBA) is defined as the artery running superficial to MN or its roots. This divergence from normal anatomy may be the possible explanation for idiopathic MN entrapment neuropathy. This study presents three cases with unilateral presence of the SBA encountered during routine undergraduate dissection at the University of Johannesburg. Case 1 - SBA divided into radial and ulnar arteries. Brachial artery (BA) terminated as deep brachial artery. Case 2 - SBA continued as radial artery (RA). BA terminated as ulnar artery (UA), anterior and posterior interosseous arteries. Case 3 - SBA continued as UA. BA divided into radial and common interosseous arteries. Arteries that take an unusual course are more vulnerable to iatrogenic injury du-ring surgical procedures and may disturb the evaluation of angiographic images during diagnosis. In particular, the presence of SBA may be acourse of idiopathic neuropathies.