Using publicly available data from three South African Development Finance Institutions (DFI's), this study examines the risk appetite of Business Partners (BP), the National Empowerment Fund (NEF) and the Small Enterprise Finance Agency (SEFA). This study analyses data between 2011 and 2015 to determine the DFI's risk appetite and to identify key determinants of risk appetite with regard to funding SMEs, specifically startups. The study's findings reveal that South African DFI's have a high to extremely high-risk appetite level and that state-owned DFI's, NEF and SEFA have a higher risk appetite for funding SMEs specifically startup related loan products than private DFI BP. The study's findings also illustrates that South African DFI's risk appetites have a weaker negative relationship with shorter-term financial products than longer-term financial products indicating a higher risk appetite for funding shorter-term financial products.

This is a book of poems.

Interest in the gut bacterial community residing in the human intestine, otherwise known as the gut microbiota, has exploded in recent years. The gut microbiome has been linked to chronic diseases such as obesity, suggesting interventions that target the microbiome may be useful in treating obesity and its complications. Dietary pulses (e.g., common beans) are composed of nutrients and compounds that possess the potential to modulate the gut bacteria composition and function which can in turn improve appetite regulation and chronic inflammation in obesity. This review summarizes the current state of knowledge regarding the connection between the gut microbiome and obesity, appetite regulation, and systemic and adipose tissue inflammation. More specifically, it highlights the efficacy of interventions employing dietary common beans as a means to improve appetite regulation and inflammation in obesity in both rodent models and in humans. Collectively, results presented and discussed herein provide insight on the gaps in knowledge necessary for a comprehensive understanding of the potential of beans as a treatment for obesity while highlighting what further research is required to gain this understanding.

In her MFA thesis “My Body Is a Question Mark Lit from Within,” Lisa Marie Schrad explores through poetry the body and its different appetites—hunger for justice, for healing, for God, for home, for wonder. Along the way, the poems also make clear that the path toward fullness and satisfaction must inevitably pass through a deep, brave commitment to knowing the full truth about ourselves. When a light shines out from inside the body, what shortcomings are exposed? What goodness is revealed? And how do we live in the world responsibly, kindly, from the space in-between our questions and their answers? In addition to these themes, Schrad offers an introduction on her understanding of poetics and reflects on what drew her to poetry even as a child.

To test the hypothesis that hypothalamic β-endorphin levels were related to the body weight changes occurring with ovarian steroid treatments, 80 adult female Sprague-Dawley rats were ovariectomized and allowed to recover for 7 days. Four treatment groups of 20 each were subjected to daily injections for 14 days with A) oil, B) β-estradiol benzoate (2µg), C) β-estradiol benzoate (2µg) plus progesterone (5mg), or D) progesterone (5mg). Weight gain was significantly (p < 0.01) lower in the estrogen group when compared to the control, estrogen/progesterone, or progesterone groups. The estrogen/progesterone-treated group gained significantly less weight than either the control or progesterone group. A significant (p < 0.05) decrease in food intake was also observed in the estrogen and estrogen/progesterone groups when compared to the control and progesterone groups, but not between each other. The progesterone-treated group was not significantly different from the controls in either weight gain or food intake. Hypothalamic β-endorphin (ng/mg protein) concentrations were significantly (p < 0.05) higher in the estrogen- and estrogen/progesterone-treated groups compared to the control and progesterone groups. Again, much like the weight gain, food intake, and hypothalamic β-endorphin (ng/mg protein), the estrogen and estrogen/progesterone groups had significantly (p < 0.05) heavier adrenal weights when compared to the controls and progesterone groups. There was no significant difference in plasma corticosterone levels between any of the groups. In this study, hypothalamic β-endorphin (ng/mg protein) appeared to be effected by ovarian steroid hormone treatment. Whether this is related to the weight gain also observed with the treatments remains to be determined. / Ph. D.

Appetite regulation is primarily mediated by the hypothalamus, within which many neurotransmitters that regulate feeding are shared by the stress response circuitry. Stressors, especially those occur during critical periods of life, influence epigenetic programming and gene expression in the long-term. Therefore, the aim of this dissertation was to elucidate how hypothalamic mechanisms of appetite regulation correlate with the stress response and epigenetic modifications, using avian models and intracerebroventricular administration of various appetite-regulating factors. We first administered two methylation modifiers, S-adenosylmethionine (SAM), a methyl donor, and 5-azacytidine (AZA), a methylation inhibitor, to determine their effects on appetite. When measuring food intake immediately post-injection, SAM didn't affect fed or fasted chickens from a line selected for low bodyweight (LWS, individuals with anorexia), but suppressed feeding in fed and fasted broilers. In Japanese quail, SAM transiently induced satiety in fed but not fasted chicks. Intriguingly, AZA increased feeding in fasted LWS but decreased it in fed chicks. While it didn't affect either fed or fasted broilers, AZA induced satiety in both fed and fasted quail. These results suggests that SAM/AZA can directly affect appetite depending on genetics and nutritional state. The LWS chickens, when injected with SAM or AZA on day of hatch, didn't show increased feeding to the orexigenic stimulation of neuropeptide Y central injection on day 5 post-hatch. This suggests that epigenetic modifications occurred following SAM/AZA injection and affect appetite regulation that persisted. In other studies, we injected broilers with prostaglandin E2 (PGE2) or β-melanocyte-stimulating hormone (β-MSH) since their effects on appetite are unknown in meat-type chicks. We found that they both potently induced satiety, but the effective duration was longer in β-MSH-injected birds (up to 9 hours) than in PGE2-injected chicks (lasted for 1.5 hours). They both activated the paraventricular nucleus of the hypothalamus. The satiety induced by β-MSH mainly involved corticotropin-releasing factor and mesotocin, while the effect of PGE2 included ghrelin and brain-derived neurotropic factor. Nevertheless, all affected appetite-related factors have connections with the stress response. Thus, our results demonstrate that the hypothalamic mechanisms underlying anorexia induced by different neuroactive molecules involve the stress response and epigenetic modifications. / Doctor of Philosophy / Eating disorders (EDs) all involve abnormal eating behaviors and altered body weight. These aberrant conditions are associated with a change in metabolism and pose great risk to human health and animal production, and are generally characterized by two opposite outcomes, anorexia and obesity. Although affected by multiple systems within the body, appetite regulation is mainly controlled by the brain, especially the hypothalamus. Thus, it is important to understand the hypothalamic mechanisms underlying the regulation of eating behavior. In the hypothalamus, many neurotransmitters affect multiple pathways, including the stress response and those that regulate appetite. Additionally, stress, especially when occurring during early life, can influence behaviors later in life through inducing epigenetic modifications (changes to the packaging of the DNA nucleotide sequence) that alter gene expression. Therefore, the aim of this dissertation was to elucidate how hypothalamic mechanisms of appetite regulation correlate with the stress response and epigenetic modifications, using avian models. To focus on the effects within the brain, we directly injected various appetite regulating factors into the brain in each of the experiments. Previously, our group demonstrated that early-life cold exposure and delayed food supply changed DNA methylation and affected expression of appetite-related genes and food intake in a chicken line predisposed to anorexia. We herein injected chicks with one of two methylation modifiers, S-adenosylmethionine (SAM), a methyl donor, and 5-azacytidine (AZA), a methylation inhibitor, to evaluate their effects on feeding behavior. When food intake was measured immediately after injection, SAM did not affect food intake in either fed or fasted line chickens from a genetic line selected for low body weight (LWS, individuals with anorexia), but suppressed food intake in both fed and fasted broiler (meat-type chickens) chicks. In Japanese quail, however, SAM only transiently induced satiety in fed chicks but not in fasted ones. Intriguingly, AZA increased food intake in fasted LWS chicks but decreased it in fed chicks, but AZA had no effects on food consumption in either fed or fasted broilers. Additionally, AZA suppressed food intake in both fed and fasted quail. These results suggest that SAM and AZA affect appetite differently depending on genetic background and nutritional states. LWS chickens, when injected with SAM or AZA on day of hatch, did not eat more after being injected with the potent hunger factor, neuropeptide Y, at 5 days of age. This indicates that epigenetic modifications occurred following SAM/AZA injection and had persisting effects on appetite regulation. In the other two studies, we injected broiler chicks with prostaglandin E2 (PGE2), a fatty acid-based molecule, or β-melanocyte-stimulating hormone (β-MSH), a peptide. These two molecules have been reported to regulate feeding behavior in rodents and layer-type chickens, but effects are unknown in broilers. They both potently decreased food intake in broilers, but the effective duration was much longer in β-MSH-injected birds (up to 9 hours) than in PGE2-injected chicks (lasted for 1.5 hours). They both activated the paraventricular nucleus of the hypothalamus, while β-MSH also activated the arcuate nucleus and ventromedial nucleus. We further found that the anorexia induced by β-MSH involved corticotropin-releasing factor, mesotocin, and their receptors, while the effect of PGE2 was associated with a change in ghrelin and brain-derived neurotropic factor gene expression. Nevertheless, all of these affected factors have connections with the stress response. Thus, results indicate that the hypothalamic mechanisms underlying anorexia induced by different neuroactive molecules involve the stress response and epigenetic modifications.

Yes / Life in a seasonally variable environment has evolved to interpret the time of year through day length (photoperiod) which is translated into a neurochemical signal. In mammals, the pars tuberalis is a key site where seasonal time signal (melatonin) interfaces and relays photoperiodic information to the hypothalamus via thyrotropin. Recent work has elucidated a potential circannual clock in ‘calendar cells’ of the pars tuberalis. In the hypothalamus, tanycytes are an integral part of the hypothalamic network. Previous studies show the importance of local synthesis of thyroid hormone and retinoic acid in tanycytes. Recently novel downstream neuroendocrine signals, e.g. VGF, FGF21 and chemerin, were identified to govern seasonally appropriate phenotype. Additionally, the hypothalamic-pituitary-growth axis has been implicated in seasonally bodyweight and torpor regulation. Here, we will focus on the endocrine drivers of photoperiod response and highlight novel downstream effects on bodyweight and growth focusing on recent findings from seasonal rodent studies.

Mammalian and avian species differ in some appetite-related aspects including how and which neurotransmitters and hormones regulate appetite. The objective of this research was to determine how two satiety-inducing neuropeptides regulate feeding behavior in avian models. Neuropeptide FF (NPFF) was intracerebroventricularly (ICV) injected into Japanese quail and decreased food intake at a dose of 32 nmol. NPFF-injected quail had increased expression levels of hypothalamic melanocortin subtype 3 receptor and decreased expression levels of neuropeptide Y receptor subtype 1 mRNAs compared to vehicle-injected controls. In a second study, gastrin was ICV injected into broiler chicks and decreased food intake at a dose of 500 ng (0.12 nmol). There was increased c-Fos immunoreactivity in the lateral hypothalamus (LH), paraventricular nucleus (PVN), arcuate nucleus, nucleus of the solitary tract, and area postrema at 1 h post-injection. Although a variety of genes were measured in those activated nuclei, there were only differences in melanin-concentrating hormone mRNA in the LH and corticotropin-releasing factor (CRF) mRNA in the PVN, suggesting that CRF signaling was involved in the hypothalamic response to gastrin. However, co-injection of gastrin and astressin, a CRF receptor antagonist did not affect gastrin-induced suppression of food intake, implying that the CRF receptors may not be directly associated with gastrin-induced satiety. Identifying the molecular pathways that mediate the effects of anorexigenic neuropeptides in birds will lead to the development of novel treatment options for appetite-related diseases and increased understanding of factors that affect production efficiency in commercial poultry and survival/resource allocation in wild birds. / Master of Science / Compulsive eating behavior associated with obesity, and anorexia nervosa, are appetite-related disorders for which no effective pharmacological treatment options exist. From an agricultural perspective, understanding what drives eating behavior is important for informing management decisions that affect animal health and welfare. From an evolutionary point of view, understanding the neural mechanisms of appetite in different species is important because of the necessity of appetite for survival. This thesis research focused on elucidating the central mechanisms associated with the actions of two neuropeptides that inhibit food intake. In the first experiment, we explored the mechanisms underlying the appetite suppressive effects of neuropeptide FF (NPFF), a neuropeptide known for its morphine-modulating properties, and found that it decreased food intake in Japanese quail, a bird that is more representative of a bird in the wild than the chicken. NPFF affected the gene expression of several appetite-related factors in the hypothalamus, a region of the brain that regulates appetite, providing insights on the associated molecular pathways. In the next study, we examined the effect of gastrin, a digestive hormone known for its role in regulating gastric acid secretion, in broiler chicks. Broiler chickens are meat-type chickens genetically selected for growth and meat production. Gastrin significantly decreased food intake in broiler chicks, and this was associated with changes in the gene expression of melanin-concentrating hormone and corticotropin-releasing factor in the lateral hypothalamus and paraventricular nucleus of the hypothalamus, respectively. Overall, we were able to provide novel insights regarding the hypothalamic mechanisms that regulate the inhibition of food consumption. These findings may lead to the development of a novel appetite suppressant or stimulant to adjust food consumption in individuals with eating disorders and chickens during specific stages of growth.

Thesis (Ph.D.)--University of Alberta, 2009. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Food Science and Technology, Department of Agricultural, Food, and Nutritional Science. Title from pdf file main screen (viewed on January 10, 2010). Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 5 uppsatser.