https://doi.org/10.1038/s41598-021-86126-0
https://pubmed.ncbi.nlm.nih.gov/33753839
Abstract
In patients with cardiovascular disorders, blood total ketone body (TKB) levels increase with worsening heart failure and are consumed as an alternative fuel to fatty acid and glucose. We investigated factors contributing to the increase in the blood TKB levels in patients with cardiovascular disorders. The study population consisted of 1030 consecutive patients who underwent cardiac catheterization. Covariance structure analyses were performed to clarify the direct contribution of hemodynamic parameters, including the left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic volume index (LVESVI), left ventricular end-diastolic volume index (LVEDVI), and B-type natriuretic peptide (BNP) levels, to TKB by excluding other confounding factors. These analyses showed that the TKB levels were significantly associated with the BNP level (P = 0.003) but not the LVEDP, LVESVI, or LVEDVI levels. This was clearly demonstrated on a two-dimensional contour line by Bayesian structure equation modeling. The TKB level was positively correlated with the BNP level, but not LVEDP, LVESVI or LVEDVI. These findings suggested that elevated blood TKB levels were more strongly stimulated by the increase in BNP than by hemodynamic deterioration. BNP might induce the elevation of TKB levels for use as an important alternative fuel in the failing heart.
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Open Access: True
Authors: Yusuke Kashiwagi - Tomohisa Nagoshi - Yasunori Inoue - Yoshiro Tanaka - Hirotake Takahashi - Yuhei Oi - Haruka Kimura - Kousuke Minai - Michihiro Yoshimura -
Additional links:
B-Type Natriuretic Peptides and Cardiac Troponins for Diagnosis and Risk-Stratification of Syncope
Jeanne du Fay de Lavallaz, Patrick Badertscher, Thomas Nestelberger, Tobias Zimmermann, Òscar Miró, Emilio Salgado, Michael Christ, Nicolas Geigy, Louise Cullen, Martin Than, F. Javier Martin-Sanchez, Salvatore Di Somma, W. Frank Peacock, Beata Morawiec, Joan Walter, Raphael Twerenbold, Christian Puelacher, Desiree Wussler, Jasper Boeddinghaus, Luca Koechlin, … Show all Authors Originally published25 Feb 2019https://doi.org/10.1161/CIRCULATIONAHA.118.038358Circulation. 2019;0
Thanks in advance
Hey all! I had a ton of blood tests done to me today at my doctor's office. I will discuss them with my doctors tomorrow. However, one of the results was for B Type Natriuetic Peptide with a value of 498 pg/mL but a standard range listed on the form was 99 pg/mL
What exactly is this? My level is nearly 5 times higher than the standard range. I plan on asking about this tomorrow too.
I am 27 year old male, that is 5'6" and weigh about 155 pounds. I'm Caucasian and take a beta blocker to help regulate my third heartbeat.
I was diagnosed with type 1 in October, and my c peptide test was very low, a test that shows how well insulin is produced, and my levels are back to normal or in the normal range. What has caused this? I am not using insulin injections for 2 months now but I only experience low blood sugars, and only occasional 170 high if I gave in to too much sweets.
http://stke.sciencemag.org/content/10/489/eaam6870
When fat is more important than muscle
>Although natriuretic peptides were originally identified as modifiers of blood pressure, they also exert metabolic effects, and obese individuals have decreased circulating natriuretic peptide concentrations. Wu et al. sought to determine whether these metabolic effects were exerted by signaling in skeletal muscle or adipose tissue. Mice with an adipose tissue–specific deficiency in the natriuretic peptide clearance receptor, which acts to limit natriuretic peptide signaling, were protected from the detrimental metabolic effects of diet-induced obesity, such as insulin resistance, inflammation, and hepatic steatosis. In contrast, mice with a muscle-specific deficiency in the clearance receptor gained weight and developed insulin resistance on a high-fat diet, similar to wild-type mice. These findings suggest that enhancing natriuretic peptide signaling in adipose tissue could be a way to counteract obesity.
Abstract
>In addition to controlling blood pressure, cardiac natriuretic peptides (NPs) can stimulate lipolysis in adipocytes and promote the “browning” of white adipose tissue. NPs may also increase the oxidative capacity of skeletal muscle. To unravel the contribution of NP-stimulated metabolism in adipose tissue compared to that in muscle in vivo, we generated mice with tissue-specific deletion of the NP clearance receptor, NPRC, in adipose tissue (NprcAKO) or in skeletal muscle (NprcMKO). We showed that, similar to Nprc null mice, NprcAKO mice, but not NprcMKO mice, were resistant to obesity induced by a high-fat diet. NprcAKO mice exhibited increased energy expenditure, improved insulin sensitivity, and increased glucose uptake into brown fat. These mice were also protected from diet-induced hepatic steatosis and visceral fat inflammation. These findings support the conclusion that NPRC in adipose tissue is a critical regulator of energy metabolism and suggest that inhibiting this receptor may be an important avenue to explore for combating metabolic disease.
Hi, I was diagnosed with type 2 in January and told to lose weight to see if it would improve my glucose. Ended up losing weight without trying to and was sick for a while. Thought i lost almost 60 pounds without effort because of other medical problems I was having at the time. Ended up falling into DKA with a glucose reading of 644 when I went into the ICU and was then diagnosed by 3 non endo doctors with type 1 diabetes due to my normal weight and young age of 20 as well as the DKA + lost weight. Just did some lab work as a follow up and got a C-peptide reading of 0.3 ng/ml with normal being 0.8-3.5 ng/ml and my glucose at the time was 105 mg/dl. Would my C-peptide indicate type 1? Or anything else ive mentioned? And does anyone know the C-peptide range for a type 2, bc I was having a hard time finding it online and EnDo doctor has rescheduled our appointment. Thank you!!
Steroidal hormones such as testosterone or cortisol as described as "hormones" and "signalling agents" of the body. Yet that's a category that's covered as well by neurotransmitters (responsible for signalling) and insulin (a peptide that also a signalling agent, and a hormone).
So what's the function of a hormone which makes it "steroidal" as opposed to other hormones like insulin?
