Endocrine control of metabolic adaptation during lactation

Vernon, Richard G.

doi:10.1079/pns19890006

Cited by 93 publications

(79 citation statements)

References 55 publications

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“…In rats, insulin resistance develops in muscle while the mammary gland becomes extremely sensitive in order to facilitate the preferential utilisation of glucose and other lipogenic precursors by the mammary gland [38,39]. By analogy, very low-carbohydrate diets during human evolution may have selected for 1283 insulin-resistant females whose metabolism conserved glucose for fetal survival and milk production.…”

Section: Metabolic Consequences Of a Low-carbohydrate High-protein Dietmentioning

confidence: 99%

The carnivore connection: dietary carbohydrate in the evolution of NIDDM

1994

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SummaryWe postulate a critical role for the quantity and quality of dietary carbohydrate in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Our primate ancestors ate a high-carbohydrate diet and the brain and reproductive tissues evolved a specific requirement for glucose as a source of fuel. But the Ice Ages which dominated the last two million years of human evolution brought a low-carbohydrate, high-protein diet. Certain metabolic adaptations were therefore necessary to accommodate the low glucose intake. Studies in both humans and experimental animals indicate that the adaptive (phenotypic) response to low-carbohydrate intake is insulin resistance. This provides the clue that insulin resistance is the mechanism for coping with a shortage of dietary glucose. We propose that the low-carbohydrate carnivorous diet would have disadvantaged reproduction in insulin-sensitive individuals and positively selected for individuals with insulin resistance. Natural selection would therefore result in a high proportion of people with genetically-determined insulin resistance. Other factors, such as geographic isolation, have contributed to further increases in the prevalence of the genotype in some population groups. Europeans may have a low incidence of diabetes because they were among the first to adopt agriculture and their diet has been high in carbohydrate for 10,000 years. The selection pressure for insulin resistance (!. e., a lowcarbohydrate diet) was therefore relaxed much sooner in Caucasians than in other populations. Hence the prevalence of genes producing insulin resistance should be lower in the European population and any other group exposed to high-carbohydrate intake for a sufficiently long period of time. [Diabetologia (1994[Diabetologia ( ) 37: 1280[Diabetologia ( -1286

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Section: Metabolic Consequences Of a Low-carbohydrate High-protein Dietmentioning

confidence: 99%

The carnivore connection: dietary carbohydrate in the evolution of NIDDM

1994

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“…Fat synthesis in adipose tissue is markedly reduced and there is usually a net loss of adipose tissue lipid (Vernon & Flint, 1984). During lactation serum glucagon does not change, serum growth hormone may rise and serum insulin, glucose and triiodothyronine concentrations are all decreased (Vernon, 1989) and in brown adipose tissue at least there is decreased sympathetic nervous activity (Trayhurn & Wusteman, 1987), all reminiscent of the fasting state. In ruminants lactation may result in an enhanced response to catecholamines and an increase in the number of P-adrenergic receptors (Vernon & Sasaki, 1991) possibly due to increased serum growth hormone levels (Watt et al 1991), but in the rat response and sensitivity to catecholamines is unchanged (Vernon & Flint, 1984).…”

Section: Effects Of Dietmentioning

confidence: 99%

Effects of diet on lipolysis and its regulation

Vernon

1992

Proc. Nutr. Soc.

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The amount of lipid in a fat cell (adipocyte) is determined by the rate of lipolysis as well as the rate of lipid synthesis. Both processes occur simultaneously and continuously, their relative rates determining if there is net lipid loss or accretion. REGULATIONS OF LIPOLYSISAcute control. Hydrolysis of triacylglycerols is catalysed by hormone-sensitive lipase. The activity of this enzyme is enhanced by phosphorylation by cyclic-AMP-dependent kinase (A-kinase). Hormone-sensitive lipase, and hence lipolysis, is thus acutely stimulated by a variety of hormones (e.g. adrenaline, glucagon, adrenocorticotrophic hormone (ACTH)) and the neurohumoral transmitter, noradrenaline, which increase the adenylate cyclase-A-kinase signal transduction system. Each peptide hormone interacts with its own receptor in the plasma membrane while adrenaline and noradrenaline interact with the P-adrenergic receptor. These hormone-receptor interactions lead to dissociation and activation of the GTP-binding protein, G,, which in turn leads to activation of adenylate cyclase (also located in the plasma membrane) and the synthesis of cyclic-AMP (Fig. 1). Cyclic-AMP activates A-kinase which in turn phosphorylates and activates hormone-sensitive lipase. Signal transduction through this system is modulated by noradrenaline and adrenaline acting via a second receptor, the 1x2-adrenergic receptor, and by prostaglandins (El and E2) and adenosine, both produced within adipose tissue, and acting via their own receptors. These receptors are coupled to a second GTP-binding protein, Gi. Receptor activation leads to dissociation of Gi which inhibits adenylate cyclase (Fig. 1). Catecholamines can, thus, both stimulate and inhibit lipolysis, the net effect depending on the relative numbers of p-and cx2-adrenergic

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“…Because of the similarity in food intake and milk yield depression, several authors have suggested that the effect of high temperature on milk production could simply be explained by a decline in nutrient supply due to reduced food intake. However, changes in the amount of nutrients in the milk do not necessarily reflect changes in the availability of dietary nutrients, since most mammals, including laboratory mice, exhibit homeorhetic (preferential) partitioning of nutrients to the mammary glands (Vernon, 1989;Vernon et al, 1999). The uptake of nutrients by mammary glands depends not only on nutrient availability but also on blood flow through the tissue, and suppression of mammary blood flow may compromise mammogenesis as well as milk secretion (Linzell, 1974;Ota and Peaker, 1979).…”

Section: Peripheral Versus Heat Dissipation Limit Hypothesesmentioning

confidence: 99%