Gender dimorphism of body mass perception and regulation in mice

Wiedmer, Petra; Boschmann, Michael; Schimrigk, К.

doi:10.1242/jeb.01120

Cited by 14 publications

(7 citation statements)

References 24 publications

(14 reference statements)

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“…This in accordance with our previous finding that the gravitostat is more effective in obese than in lean mice 3 . In line with this, there were only small and inconsistent effects of loading in lean animals in some early studies 30,31 . Very recently, we also found that loading is effective in suppressing body weight in obese humans 2 .…”

Section: Discussionsupporting

confidence: 92%

The gravitostat protects diet‐induced obese rats against fat accumulation and weight gain

Bake

Peris-Sampedro

Wáczek

et al. 2021

J Neuroendocrinology

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The gravitostat is a novel homeostatic body weight‐regulating mechanism, mostly studied in mice, and recently confirmed in obese humans. In the present study, we explored the effect of weight loading on metabolic outcomes, meal patterns and parameters linked to energy expenditure in both obese and lean rats. Diet‐induced obese (DIO) and lean rats were implanted with capsules weighing either 15% of biological body weight (load) or empty capsules (1.3% of body weight; controls). Loading protected against fat accumulation more markedly in the DIO group. In line with this, the obesity‐related impairment in insulin sensitivity was notably ameliorated in DIO rats upon loading, as revealed by the reduction in serum insulin levels and homeostatic model assessment for insulin resistance index scores. Although 24‐hour caloric intake was reduced in both groups, this effect was greater in loaded DIO rats than in loaded lean peers. During days 10‐16, after recovery from surgery, loading: (i) decreased meal size in both groups (only during the light phase in DIO rats) but this was compensated in lean rats by an increase in meal frequency; (ii) reduced dark phase locomotor activity only in lean rats; and (iii) reduced mean caloric efficiency in DIO rats. Muscle weight was unaffected by loading in either group. Dietary‐obese rats are therefore more responsive than lean rats to loading.

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Section: Discussionsupporting

confidence: 92%

The gravitostat protects diet‐induced obese rats against fat accumulation and weight gain

Bake

Peris-Sampedro

Wáczek

et al. 2021

J Neuroendocrinology

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“…If this is the case, female mice, which have a much lower level of testosterone, should show a higher body weight and fasting blood glucose level compared with male mice. However, the fact is that the normal female mice generally show lower body weight than male mice ( 28 , 29 , 30 ). There are sex differences in the body weight variation and distribution, energy conversion to body weight, and body composition changes ( 28 ), which may be contributed by estrogen level ( 31 ), sex-specific leptin resistance ( 32 , 33 ), and differences in gross locomotor activity ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Mice lacking the proton channel Hv1 exhibit sex-specific differences in glucose homeostasis

Pang

Li²,

Wang

et al. 2021

Journal of Biological Chemistry

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Sex as a physiologic factor has a strong association with the features of metabolic syndrome. Our previous study showed that loss of the voltage-gated proton channel Hv1 inhibits insulin secretion and leads to hyperglycemia and glucose intolerance in male mice. However, there are significant differences in blood glucose between male and female Hv1-knockout (KO) mice. Here, we investigated the differences in glucose metabolism and insulin sensitivity between male and female KO mice and how sex steroids contribute to these differences. We found that the fasting blood glucose in female KO mice was visibly lower than that in male KO mice, which was accompanied by hypotestosteronemia. KO mice in both sexes exhibited higher expression of gluconeogenesis-related genes in liver compared with WT mice. Also, the livers from KO males displayed a decrease in glycolysis-related gene expression and an increase in gluconeogenesis-related gene expression compared with KO females. Furthermore, exogenous testosterone supplementation decreased blood glucose levels in male KO mice, as well as enhancing insulin signaling. Taken together, our data demonstrate that knockout of Hv1 results in higher blood glucose levels in male than female mice, despite a decreased insulin secretion in both sexes. This sex-related difference in glucose homeostasis is associated with the glucose metabolism in liver tissue, likely due to the physiological levels of testosterone in KO male mice.

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“…However, animals are also able to directly sense their own body weight, possibly via mechano-sensors in the joints and limbs. For example, if inert weights are implanted into the body cavities of small mammals they rapidly adjust their tissue mass to compensate for their increased body weight (Adams et al, 2001;Wiedmer et al, 2004).…”

Section: Physiological Consequences Of the Disease-predation Dualintementioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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Human obesity has a large genetic component, yet has many serious negative consequences. How this state of affairs has evolved has generated wide debate. The thrifty gene hypothesis was the first attempt to explain obesity as a consequence of adaptive responses to an ancient environment that in modern society become disadvantageous. The idea is that genes (or more precisely, alleles) predisposing to obesity may have been selected for by repeated exposure to famines. However, this idea has many flaws: for instance, selection of the supposed magnitude over the duration of human evolution would fix any thrifty alleles (famines kill the old and young, not the obese) and there is no evidence that hunter-gatherer populations become obese between famines. An alternative idea (called thrifty late) is that selection in famines has only happened since the agricultural revolution. However, this is inconsistent with the absence of strong signatures of selection at single nucleotide polymorphisms linked to obesity. In parallel to discussions about the origin of obesity, there has been much debate regarding the regulation of body weight. There are three basic models: the setpoint, settling point and dual-intervention point models. Selection might act against low and high levels of adiposity because food unpredictability and the risk of starvation selects against low adiposity whereas the risk of predation selects against high adiposity. Although evidence for the latter is quite strong, evidence for the former is relatively weak. The release from predation ∼2-million years ago is suggested to have led to the upper intervention point drifting in evolutionary time, leading to the modern distribution of obesity: the drifty gene hypothesis. Recent critiques of the dual-intervention point/ drifty gene idea are flawed and inconsistent with known aspects of energy balance physiology. Here, I present a new formulation of the dual-intervention point model. This model includes the novel suggestion that food unpredictability and starvation are insignificant factors driving fat storage, and that the main force driving up fat storage is the risk of disease and the need to survive periods of pathogen-induced anorexia. This model shows why two independent intervention points are more likely to evolve than a single set point. The molecular basis of the lower intervention point is likely based around the leptin pathway signalling. Determining the molecular basis of the upper intervention point is a crucial key target for future obesity research. A potential definitive test to separate the different models is also described.

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Gender dimorphism of body mass perception and regulation in mice

Cited by 14 publications

References 24 publications

The gravitostat protects diet‐induced obese rats against fat accumulation and weight gain

The gravitostat protects diet‐induced obese rats against fat accumulation and weight gain

Mice lacking the proton channel Hv1 exhibit sex-specific differences in glucose homeostasis

The evolution of body fatness: trading off disease and predation risk

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