Effects of fasting and refeeding on <i>ob</i> gene expression in white adipose tissue of lean and obese (<i>ob/ob</i>) mice

doi:10.1016/0014-5793(95)00719-p

Cited by 243 publications

(29 citation statements)

References 9 publications

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“…In this model, increased hypothalamic-pituitary-adrenal axis activity, which occurs secondary to an acquired leptin deficiency, is also necessary (40–44). In our hands (45) and others’ (8, 46–68), plasma leptin concentrations and WAT leptin expression have been shown to drop quickly with starvation. To understand the role of this reduction in plasma leptin, Ahima et al performed a classic study in which they performed an intraperitoneal injection of leptin resulting in plasma leptin concentrations initially 100 times normal, and examined various physiologic parameters twelve hours later.…”

Section: Introduction: Leptin and Starvationsupporting

confidence: 58%

The Role of Leptin in Maintaining Plasma Glucose During Starvation

Perry¹,

Shulman²

2018

PDJ

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For 20 years it has been known that concentrations of leptin, a hormone produced by the white adipose tissue (WAT) largely in proportion to body fat, drops precipitously with starvation, particularly in lean humans and animals. The role of leptin to suppress the thyroid and reproductive axes during a prolonged fast has been well defined; however, the impact of leptin on metabolic regulation has been incompletely understood. However emerging evidence suggests that, in starvation, hypoleptinemia increases activity of the hypothalamic-pituitary-adrenal axis, promoting WAT lipolysis, increasing hepatic acetyl-CoA concentrations, and maintaining euglycemia. In addition, leptin may be largely responsible for mediating a shift from a reliance upon glucose metabolism (absorption and glycogenolysis) to fat metabolism (lipolysis increasing gluconeogenesis) which preserves substrates for the brain, heart, and other critical organs. In this way a leptin-mediated glucose-fatty acid cycle appears to maintain glycemia and permit survival in starvation.

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Section: Introduction: Leptin and Starvationsupporting

confidence: 58%

The Role of Leptin in Maintaining Plasma Glucose During Starvation

Perry¹,

Shulman²

2018

PDJ

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“…Leptin is predominantly secreted from visceral white adipocytes in rodents 40 and from subcutaneous adipose tissue in humans 41 . There is a general consensus that leptin levels are tightly correlated with adiposity in both rodents and humans 42 .…”

Section: Leptin and Adipose Functionsmentioning

confidence: 99%

“…For instance, both Lep expression and circulating leptin levels show a circadian rhythm; in rats, they peak during the late-dark, active period ( 21) and reach their nadir during the late-light, inactive period (zeitgeber time 9) 44 . However, the changes in leptin expression across the circadian cycle are very modest (about 1.5-fold) 44 compared with changes in response to metabolic challenges (such as fasting or cold exposure), which rapidly affect leptin synthesis independent of changes in fat mass 26,40,45 (FIG. 2).…”

Section: Leptin and Adipose Functionsmentioning

confidence: 99%

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Leptin and brain–adipose crosstalks

et al. 2018

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Interactions between the brain and distinct adipose depots have a key role in maintaining energy balance, thereby promoting survival in response to metabolic challenges such as cold exposure and starvation. Recently, there has been renewed interest in the specific central neuronal circuits that regulate adipose depots. Here, we review anatomical, genetic and pharmacological studies on the neural regulation of adipose function, including lipolysis, non-shivering thermogenesis, browning and leptin secretion. In particular, we emphasize the role of leptin-sensitive neurons and the sympathetic nervous system in modulating the activity of brown, white and beige adipose tissues. We provide an overview of advances in the understanding of the heterogeneity of the brain regulation of adipose tissues and offer a perspective on the challenges and paradoxes that the community is facing regarding the actions of leptin on this system.

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“…Even for leptin concentrations in blood, the role of glucose is controversial, largely because of the confounding effects of glucose-stimulated insulin production [15, 16, 17]. Although both fasting and streptozotocin (STZ)-induced diabetes mellitus are characterized by reduced concentrations of leptin and insulin in blood as well as markedly down-regulated ob mRNA in adipose tissue, only STZ causes hyperglycemia [13, 15, 16, 18, 19, 20, 21]. …”

Section: Introductionmentioning

confidence: 99%

Glucose and Insulin Increase the Transport of Leptin through the Blood-Brain Barrier in Normal Mice but Not in Streptozotocin-Diabetic Mice

Kastin

Akerstrom²

2001

Neuroendocrinology

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Since fasting is one of the few factors found to change the rate of entry of leptin into brain, we used multiple-time regression analysis to study the effects of pretreatment with glucose or insulin on leptin transport across the blood-brain barrier (BBB). Two hours after intraperitoneal injection of glucose (3 g/kg), there was a statistically significant increase in the entry rate (K_i) of leptin in fasted (from 4.91 ± 0.70 × 10^–4 ml/g min to 9.03 ± 1.00 × 10^–4 ml/g min) but not (p = 0.15) in nonfasted normal (from 4.90 ± 1.21 × 10^–4 ml/g min to 6.42 ± 1.79 × 10^–4 ml/g min) or fasted streptozotocin (STZ)-treated diabetic mice (from 4.043 ± 0.959 × 10^–4 ml/g min to 5.395 ± 1.355 × 10^–4 ml/g min). Insulin (10 U/kg) increased leptin influx in fasted (from 4.77 ± 0.26 × 10^–4 ml/g min to 10.6 ± 0.15 × 10^–4 ml/g min at 0.5 h) and nonfasted (from 4.64 ± 0.75 × 10^–4 ml/g min to 7.46 ± 1.48 × 10^–4 ml/g min at 0.5 h) normal mice, but not in STZ-diabetic mice deficient in insulin (and leptin), even though basal concentrations of glucose were similarly increased in the nonfasted normal and STZ-treated mice. Moreover, the basal rate of leptin influx was the same in overnight fasted normal mice, nonfasted normal mice and STZ-diabetic mice. The results indicate that glucose and insulin can increase leptin transport, but they probably are not the principal factors responsible for the regulatory effect of the BBB on leptin entry into the brain.

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Effects of fasting and refeeding on ob gene expression in white adipose tissue of lean and obese (ob/ob) mice

Cited by 243 publications

References 9 publications

The Role of Leptin in Maintaining Plasma Glucose During Starvation

The Role of Leptin in Maintaining Plasma Glucose During Starvation

Leptin and brain–adipose crosstalks

Glucose and Insulin Increase the Transport of Leptin through the Blood-Brain Barrier in Normal Mice but Not in Streptozotocin-Diabetic Mice

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