The Covid19 pandemic should be seen as a wake-up call for humanity, to reflect, rethink and redesign food systems that are safe, healthy, sustainable, and beneficial to all. This crisis has disrupted food supply chains, affecting lives and livelihoods. Hunger and malnutrition is expected to increase and the poor and vulnerable will suffer the most. There is urgent need to build resilient food systems. A location specific farm-system-for-nutrition approach, based on sustainable use of natural resources and local agri-food value chains can help improve household diet diversity and address nutrition deficiencies. The food-based approach can improve preparedness and resilience of communities to withstand the challenge posed by crises in general, and COVID19 in particular.

The urinary excretion of N tau-methylhistidine (N tau-MH) was studied quantitatively in growing Hereford steers to measure muscle protein degradation (MPD) at different stages of growth. The amount of MPD and the fractional rate of protein breakdown (FBR) on 28, 42, 56 and 63 d of the experiment were calculated from the 24-h urinary N tau-MH excretion. The steers grew rapidly during the initial phase of the study; the growth rate was higher on d 56 (P less than .01) than on d 42 of the study. On d 63, there was a reduction in the growth rate compared with d 56 (P less than .05). Daily urinary N tau-MH excretion increased gradually as the animals gained weight and on an average, it was 1,957 +/- 88 mumol/d during the entire experimental period. Urinary creatinine excretion was not different at different growth stages, but the urinary N tau-MH: creatinine ratio was higher (P less than .05) on d 56 than on the other days. The amount of MPD per day increased gradually as the animals gained weight and was higher on d 56 than on d 42. Mean MPD and FBR values during the entire experimental period were 557 +/- 25 g/d and 2.44 +/- .09%/d, respectively. Half-life of the myofibrillar proteins decreased as the steers gained weight. These results indicate that the rapid growth in steers is accompanied by a high rate of MPD and demonstrate the usefulness of urinary N tau-MH excretion as a rapid, nondestructive method for measuring muscle protein degradation in large animals.

The effects of a porcine insulin-like growth factor (IGF)-binding protein on binding of IGF-I and IGF-II to porcine aortic endothelial cells (PAEC) were determined. Binding of 125I-labelled IGF-I and -II to IGF receptors was inhibited by IGF-binding protein. IGF-binding protein inhibited binding of IGF-I and -II in a dose-dependent manner with half-maximal inhibition occurring at 5.43 and 108 micrograms/l respectively. A 125I-labelled IGF-I--IGF-binding protein complex, formed by incubating 125I-labelled IGF-I with IGF-binding protein overnight at 4 degrees C, did not effectively bind to endothelial IGF receptors. Addition of IGF-binding protein to PAEC previously incubated with IGF-I caused a marked dissociation of bound IGF-I (47% dissociation within 12h). These results indicate that the acid-stable IGF-binding protein which appears to be a part of the 150 kDa GH-dependent binding protein, blocks binding of IGF-I and -II by the IGF receptors and appears to exhibit a higher affinity for IGF-I than the endothelial type-I IGF receptor. The ramifications of this latter point with respect to transfer of circulating IGFs (bound to their IGF-binding proteins) across the vascular endothelium are not clear.

This study was conducted to determine whether the increase in serum glucose observed in pigs treated chronically with pGH is due to an increase in hepatic glucose output or to an impairment in glucose clearance. Barrows (n = 4 per treatment) were treated with pituitary derived pGH (ppGH), recombinant pGH analog (rpGH) or vehicle. Pigs were treated for 28 d by daily i.m. injections. Insulin tolerance and glucose tolerance tests (GTT) were performed on d 19 and 21, respectively, following treatment with pGH. Glucose turnover was quantified on d 28 using [6-3H]glucose. Chronically treating pigs with pGH resulted in a significant decrease (26%; P less than .05) in glucose clearance, as determined by the GTT. Glucose clearance was affected similarly by ppGH and rpGH. Intra-arterial glucose infusion markedly increased plasma insulin concentration in pGH-treated pigs. Peak plasma insulin response was 87% and 58%, respectively, higher (P less than .05) in ppGH- and rpGH-treated than in control pigs. Insulin infusion elicited a marked hypoglycemia in pigs; however, the extent and duration of hypoglycemia were significantly less in pGH-treated pigs (ppGH or rpGH). Glucose production rates were 23% higher (P = .085) in ppGH-treated than in control pigs. These results establish that the hyperglycemia induced by pGH is the result of an increase in hepatic glucose output and a concurrent impairment in glucose clearance.

The acute and chronic effects of porcine growth hormone (pGH) administration on glucose homeostasis of pigs were investigated in the present study. Twelve Yorkshire barrows (average BW = 65 kg) fitted with femoral artery catheters were allotted to three groups. Pigs received acute, intra-arterial injections of either pituitary pGH, a recombinantly derived pGH analog (ppGH or rpGH, 100 micrograms/kg BW) or saline. Acute injection of pGH did not affect fasting plasma glucose or insulin status. Pigs then were treated daily by i.m. injection for 24 d with 70 micrograms ppGH/kg BW. Serum glucose and insulin concentrations during the fed and fasted states were higher in pGH-treated than in control pigs. On d 25, an acute intra-arterial injection of ppGH (100 micrograms/kg BW) elicited increases in plasma glucose and insulin in pigs chronically treated with pGH. The area circumscribed by the glucose and insulin response curves 5 min to 7 h postinjection was 40% (P less than .005) and 177% (P less than .001), respectively, higher in ppGH-treated than in control pigs. These data indicate that pGH does increase plasma glucose and insulin in the fed and fasted states; however, this response is only observed after chronic pGH administration. In addition, pGH is capable of increasing plasma glucose and insulin acutely in the pig. This effect, however, only is observed in pigs treated chronically with pGH. The mechanisms by which pGH elicit these effects on glucose homeostasis are not known.