Link to 2005 article
by MacLean, Higgins, Giles, Sherk, and Jackman
"What complicates the role of leptin and insulin as ‘adipose signals’ is that their relationship
to adiposity is maintained only during energy balance and
the correlations only apply to fasted levels of the hormones.
When an energy imbalance occurs, leptin and insulin
reflect the metabolic state (anabolic or catabolic) of adipose tissue,
as it deposits or mobilizes energy.
Overfeeding increases circulating levels of leptin and insulin 93 and,
with persistent overfeeding during weight regain, both leptin and insulin
resolve long before the weight is fully regained 7.
For this reason, leptin and insulin, by themselves,
do not appear to sustain the signal of energy depletion as weight is being regained."
From a figure in this article:to adiposity is maintained only during energy balance and
the correlations only apply to fasted levels of the hormones.
When an energy imbalance occurs, leptin and insulin
reflect the metabolic state (anabolic or catabolic) of adipose tissue,
as it deposits or mobilizes energy.
Overfeeding increases circulating levels of leptin and insulin 93 and,
with persistent overfeeding during weight regain, both leptin and insulin
resolve long before the weight is fully regained 7.
For this reason, leptin and insulin, by themselves,
do not appear to sustain the signal of energy depletion as weight is being regained."
"Adipocyte cellularity changes with weight loss and weight regain.
Representative adipocytes are shown in the context of obesity,
after weight loss and after weight regain.
Weight loss would reduce the average size of resident adipocytes.
Weight regain could involve both hypertrophy and hyperplasia.
Changes in the neuroendocrine inputs (SNS tone and T3)
that may be contributing to the adaptive response to weight loss
are shown for each metabolic context.
Likewise, changes in the secretion of the long-term adipose signal reflecting stored energy
(leptin and insulin) are shown for each metabolic context.
Finally, the systemic impact on nutrient availability is presented
as the relative flux of glucose, triglycerides (TG) and free fatty acids (FFA).
Both long-term (leptin) and short-term (nutrients and their surrogate signals)
would be sensed by the hypothalamus and hindbrain
to regulate appetite and metabolic requirements.
This article puts a question mark about the effect of hyperplasia (number of fat cells)
The Chronic Obese have a great number of adipocytes that never die.
I believe the ratio of the number of adipocytes vs. the leptin level cause regain
with hunger and decreased thermogenesis
that does persist as the number of fat cells is not decreased. The Sponge Syndrome.
Representative adipocytes are shown in the context of obesity,
after weight loss and after weight regain.
Weight loss would reduce the average size of resident adipocytes.
Weight regain could involve both hypertrophy and hyperplasia.
Changes in the neuroendocrine inputs (SNS tone and T3)
that may be contributing to the adaptive response to weight loss
are shown for each metabolic context.
Likewise, changes in the secretion of the long-term adipose signal reflecting stored energy
(leptin and insulin) are shown for each metabolic context.
Finally, the systemic impact on nutrient availability is presented
as the relative flux of glucose, triglycerides (TG) and free fatty acids (FFA).
Both long-term (leptin) and short-term (nutrients and their surrogate signals)
would be sensed by the hypothalamus and hindbrain
to regulate appetite and metabolic requirements.
This article puts a question mark about the effect of hyperplasia (number of fat cells)
The Chronic Obese have a great number of adipocytes that never die.
I believe the ratio of the number of adipocytes vs. the leptin level cause regain
with hunger and decreased thermogenesis
that does persist as the number of fat cells is not decreased. The Sponge Syndrome.
Back to the article:
"Once the adipocytes near a critical threshold of size
and the maximal capacity for stored energy is approached,
the rate of weight regain would diminish.
As the pre‐weight loss weight is once again achieved, or surpassed if adipocyte hyperplasia
has occurred, the fasting and postprandial levels of circulating nutrients
would once again reflect the high levels observed with the insulin resistant state."
Brian Edwards MD Pertinent article below:
"Once the adipocytes near a critical threshold of size
and the maximal capacity for stored energy is approached,
the rate of weight regain would diminish.
As the pre‐weight loss weight is once again achieved, or surpassed if adipocyte hyperplasia
has occurred, the fasting and postprandial levels of circulating nutrients
would once again reflect the high levels observed with the insulin resistant state."
Brian Edwards MD Pertinent article below:
"In LEAN individuals high insulin and leptin prevent weight gain, not IR. In OBESE Insulin triggers SF1 expressing neurons of VHM resulting in inhibition of POMC which promotes food intake & perpetuates obesity"
Trends Endocrinol Metab. 2013 Feb;24(2):76-84. Vogt MC1, Brüning JC.
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